College Directory

    Dr. Griff Parks
  • Title: Interim Associate Dean of Research; Director, Burnett School of Biomedical Sciences and Professor
  • Office: BBS 101G
  • Phone: 407.266.7011
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  • Biography:

    We study the replication and innate immune responses to Paramyxoviruses – a remarkably diverse family of negative-strand RNA viruses, some of which are the most ubiquitous disease-causing viruses of humans and animals. This work includes the development of vectors for therapy or vaccination that are based on novel properties of the viral genomes and proteins. In addition, we have expanded our focus to include viral immunology projects (interferon and complement) with the bioterrorism agent Nipah virus and the pathogenic bunyaviruses.

    Our lab projects can be divided into three general areas:

    1)    Interactions of negative strand RNA viruses with interferon and complement immune pathways. We address the questions of how these viruses first activate and then suppress important innate immune pathways in order to successfully replicate. This involves studies to understand the viral factors that induce interferon and complement responses, as well as the cellular sensors and pathways that respond, suppress replication, and neutralize virus.

    2)    Developing of novel viral vectors for tumor therapy. We are taking advantage of inherent properties of the viruses we study to design novel vectors for controlled killing of tumor cells. This includes modifying the viral glycoproteins to produce vectors with enhanced ability to spread through a population of tumor cells. In addition, viral mutants which are defective in suppression of innate immunity are being tested for their ability to spread in tumor cells while retaining restricted growth in normal cells.

    3)    Development of vaccine vectors based on paramyxoviruses. Viral vectors can be potent inducers of innate and adaptive immunity, but also can cause disease in some cases. We are exploiting unique properties of some of these paramyxoviruses to develop new delivery vehicles that balance attenuated replication with induction of strong immunity to an engineered antigen.

    Recent Publications

    1. Ganguli T, Johnson JB, Parks GD and Deora R. 2014. Bordetella BPS interactions with human complement pathways. Cellular Microbiol 16:1105-1118.
    2. Mayer AE, Johnson JB, and Parks GD. 2014. The neutralizing capacity of antibodies elicited by parainfluenza virus infection of African Green monkeys is dependent on complement. Virology 460:23-33.
    3. Khalil SM, Tonkin DR, Snead AT, Parks GD, Johnston RE, and White LJ. 2014. An alphavirus-based adjuvant enhances serum and mucosal antibodies, T cells and protective immunity to influenza virus in neonatal mice. J. Virol. 88:9182-9196.
    4. Johnson JB, Schmitt AP, and Parks GD. 2013. Point mutations in the paramyxovirus F protein that enhance fusion activity shift the mechanism of complement-mediated virus neutralization. J. Virol 87:9250-9259
    5. Parks GD and Alexander-Miller MA. 2013. Invited Review: Paramyxovirus activation and inhibition of innate immune pathways. J. Molec. Biol. 425:4872-4892.
    6. Johnson JB, Lyles DS, Alexander-Miller MA and Parks GD. 2012. Virion-associated CD55 is more potent than CD46 in mediating resistance of mumps virus and VSV to neutralization. J. Virol. 86:9929-9940.
    7. Biswas, M, Kumar S, Johnson J, Parks GD and Subbiah E. 2012. Incorporation of host complement regulatory proteins into Newcastle Disease virus enhances complement evasion. J. Virol. 86:12708-12716.
    8. Briggs CM and Parks GD. 2012. Mumps virus inhibits migration of primary human macrophages toward a chemokine gradient through a TNF-alpha dependent mechanism. Virology 433:245-252.
    9. Johnson JB, Aguilar H, Lee B, and Parks GD. 2011. Interactions of human complement with virus particles containing the Nipah virus glycoproteins. J. Virol. 85:5940-5948.
    10. Clark KM, Johnson JB, Kock ND, Mizel SB and Parks GD. 2011. Parainfluenza virus 5-based vaccine vectors expressing vaccinia virus VACV antigens provide long-term protection in mice from lethal intranasal VACV challenge. Virology 419:97-106.
    11. Briggs CM, Holder RC, Reid SD and Parks GD. 2011. Activation of human macrophages by bacterial components relieves the restriction on replication of an interferon-inducing parainfluenza virus 5 (PIV5) P/V mutant. Microbes and Infection. 13:359-368.
    12. Manuse MJ and Parks GD. 2010. TLR3-dependent upregulation of RIG-I leads to enhanced cytokine production from cells infected with the parainfluenza virus SV5. Virology 397: 231-241.
    13. Armilli S, Sharma SK, Yammani R, Reid SD, Parks GD, and Alexander-Miller MA. 2010. Nonfunctional lung effectors exhibit decreased calcium mobilization associated with reduced expression of ORAI1. J. Leuk Biol. 87:977-88.
    14. Manuse MJ, Briggs CM, and Parks GD. 2010. Replication-Independent activation of human plasmacytoid dendritic cells by the paramyxovirus SV5 requires TLR7 and autophagy pathways. Virology 405:383-389.
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    Dr. Raheleh Ahangari
  • Title: Assistant Professor
  • Office: HPA II 321
  • Phone: 407-823-1793
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  • Biography:

     

    Dr. Raheleh Ahangari is an Assistant Professor of Medicine (teaching position) in Burnett School of Biomedical Sciences at UCF College of Medicine and is teaching Human Physiology, Clinical Embryology and Clinical Endocrinology.

    She received her Doctor of Medicine (M.D.) degree from Carol Davilla Medical University, Bucharest, Romania (1987- 1993) and took several graduate neuroscience courses in the department of Cell Biology and Pathology in the Faculty of Medicine in University of Salamanca to receive “Sufficient Investigator” status in her graduate studies (1997- 1999) where she carried out research in trigeminal neuralgia and headache under supervision of Dr. Rafael Covenas. She then moved to Germany for a post-doc position in Wuerzburg, Germany in 2000. Her studies focused on immunology, looking for signal transduction mechanisms in apoptosis and T-cell proliferation in department of immunology-virology (supervisor: Dr. U. Bommhardt) of Wuerzburg University (2000). She continued her post-doc studies on Macro-patch-clamp recording of the hemi-diaphragm, to characterize the receptors involved in neurotransmission including pre- and post- synaptic molecules involved in the pathogenesis of Guillain Barré syndrome (GBS) and Miller Fischer syndrome in 2001-2002 (Supervisors: Dr. B. Buchwald and Dr. C.V. Toyka, head of the neurology university hospital).

    In 2003, she received an Assistant Professor position in Anatomy in Saba university school of medicine, Saba, Netherlands-Antilles, and moved to the United States in Aug. 2004. She joined UCF as a teaching faculty in fall 2005 and got involved in research in Dr. H. Daniell’s lab, looking for therapeutic effects of oral delivery of pro-insulin conjugated to cholera toxin-B subunit produced in tobacco and lettuce fed to diabetic mice (2005- 2006). Dr. Ahangari co-developed clinical embryology and congenital malformations as well as clinical endocrinology courses in UCF in 2006 and teaching them since then.

    Dr. Ahangari is a graduate faculty scholar and has directed several independent studies in endocrine and metabolic disorders and was involved in a number of honors in major thesis works. Her research/scholarly activities are focused on trigeminal neuralgias and headache as well as inflammation. She is a Co-PI of a SBIR research with Dr. P. Mangos from Adaptive Immersion Technologies,  working on the development of a Holographic Health Avatar for Predictive and Preventative Medicine (2016-2017).

     

    PUBLICATIONS

    1. Samsam M, Ahangari R. Neuromodulation in the treatment of migraine: Progress in nerve stimulation. Neuro Open J. 2017; 3(1): 9-22. doi:10.17140/NOJ-3-122.
    2. Samsam M., Ahangari R., Naser SA.: Pathophysiology of autism spectrum disorders: Revisiting gastrointestinal involvement and immune imbalance. World J Gastroenterol. 2014 Aug 7;20 (29):9942-9951.
    3. Samsam M., Coveñas R., Ahangari R., Yajeya J.: Neuropeptides and other chemical mediators, and the role of anti-inflammatory drugs in primary headaches, AIAA-MC, 2010, 3: 170- 188.
    4. Samsam M., Coveñas R., Ahangari R., Yajeya J.: Major neuroanatomical and neurochemical substrates involved in primary headaches. In: Neuroanatomy Research Advances; chapter 1; Editors: CE Flynn and BR Callaghan; Nova Science Publishers; New York; 2009; pp1- 58; ISBN: 978-60741-610-4.
    5. Samsam M., Coveñas R., Ahangari R., Yajeya J. and Narváez JA.: Role of neuropeptides in migraine headaches, experimental and clinical data, Focus on Neuropeptide Research, chapter 11; Editor: R. Covenas; Transworld Research Network; India, released in 2008; ISBN: 978-81-7895-291-8.
    6. Samsam M., Coveñas R., Ahangari R., Yajeya J. and Narváez JA: Role of neuropeptides in migraine; where do they stand in the latest expert recommendations in migraine treatment? Drug Development Research, 2007, 68: 298- 314.
    7. Ruhlman T., Ahangari R., Devine A., Samsam M. and Daniell H.: Expression of cholera toxin B-proinsulin fusion protein in lettuce and tobacco chloroplasts – oral administration protects against development of insulitis in non-obese diabetic mice, Plant Biotechnol J., 2007, 5: 495- 510.  *Shared first authorship
    8. Buchwald B., Ahangari R., Weishaupt A. and Toyka C.V.: Presynaptic effects of immunoglobulin G from patients with Lambert Eaton Myasthenic syndrome: their neutralization by intravenous immunoglobulins, Muscle Nerve, 2005, 31: 487-94.
    9. Samsam M., Coveñas R, Ahangari R., Yajeya J, Narváez J.A., Montes C. and González-Barón S.: Implications of somatostatin, neurotensin and methionin-enkephalin in an experimental model of headache. Neurol.,  2002, 34: 724- 729.
    10. Buchwald B., Ahangari R., Weishaupt A. and Toyka KV.: Intravenous immunoglobulins neutralize blocking antibodies in Guillain-Barré syndrom, Ann. , 2002, 51: 673- 680.
    11. Buchwald B., Ahangari R. and Toyka KV.: Differential blocking effects of the monoclonal anti-GQ1b IgM antibody and alpha-latrotoxin in the absence of complement at the mouse neuromuscular junction, Neurosci. Let., 2002, 334: 25- 28.
    12. Samsam M., Coveñas R, Csillik B., Ahangari R., Yajeya J, Riquelme R., Narváez J.A. and Tramu G.: Depletion of substance P, neurokinin A and calcitonin geme-related peptide from the contralateral caudal trigeminal nucleus following a unilateral electrical stimulation of the trigeminal ganglion; the functional neuroanatomy underlying the clinical manifestaion of generalized migraine headaches. Chem. Neuroanatomy, 2001, 21: 161- 169.
    13. Samsam M., Coveñas R., Ahangari R., Yajeya J., Narváez J.A., Tramu G.: Simultaneous depletion of neurokinin A, substance P and calcitonin gene related peptide immunoreactivities in the caudal trigeminal nucleus of the rat following electrical stimulation of the Gasserian ganglion: a possible co-release of neuropeptides. PAIN, 2000, 84: 389- 395.
    14. Samsam M., Coveñas R., Ahangari R., Yajeya J., Riquelme R. and Narváez J.A.: Changes in neuropeptide distribution in the caudal trigeminal nucleus following electrical stimulation of the trigeminal ganglion: an experimental migraine model. MAPFRE MEDICINA ESPANA, 2000, 11/2: 111- 118.
    15. Samsam M., Coveñas R., Ahangari R., Yajeya J., Narváez J.A., Tramu G.: Neurokinin A and Substance P and calcitonin gene-related peptide immunoreactivities in the rat caudal trigeminal ganglion. Neurosci. Let.,1999, 261: 1-4.
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    Dr. Salvador Almagro-Moreno
  • Title: Assistant Professor
  • Office: BMS 125A
  • Phone: 407.823.3982; 407.823.3987 (lab)
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  • Biography:

    Our primary scientific interest lies at the interface between ecology and pathogenesis. We investigate how environmental factors affect the pathogenic potential of marine bacteria, which genetic traits are prerequisites in colonizing a new niche such as the human host, how they acquire and regulate virulence genes, and what are their ecological relationships with other members of their natural environment and the host’s microbiota.

    We study members of the family Vibrionaceae, a highly diverse group of marine bacteria that includes from symbionts to human pathogens. Some of the species we work with include Vibrio cholerae, the etiological agent of the severe diarrheal disease cholera, Vibrio vulnificus, an emergent pathogen that causes a deadly septicemia, and Vibrio coralliilyticus, a coral pathogen whose emergence is linked to climate change.

    Our research approach strives to be holistic and multidisciplinary; what we call “From Bays to Bases”. It encompasses a mix of molecular biology, genomics, phylogenetics, pathogenesis, and ecology. We believe that by understanding pathogen evolution and ecology we will ultimately gain the knowledge that will allow us to forecast the traits of emergent virulent strains, predict the sources of outbreaks, and to design and produce affordable and safe vaccines and reliable treatments against bacterial threats.

    Learn more about my lab atwww.vibriocholerae.org

    Recent Publications

     

    1. Bile salts and alkaline pH reciprocally modulate the interaction between the periplasmic domains of Vibrio cholerae ToxR and ToxS
    C. R. Midgett, S. Almagro-Moreno, M. Pellegrini, R. K. Taylor, K. Skorupski, F. J. Kull. Molecular Microbiology. 2017

    2. Origins of pandemic clones from environmental gene pools
    B. J. Shapiro, I. Levade, G. Kovacikova, R. K. Taylor, S. Almagro-Moreno*. Nature Microbiology. 2016

    3. Intestinal colonization dynamics of Vibrio cholerae
    S. Almagro-Moreno*, K. Pruss, and R. K. Taylor. PLoS Pathogens. 2015

    4. Proteolysis of virulence regulator ToxR is associated with entry of Vibrio cholerae into a dormant state
    S. Almagro-Moreno*, T. K. Kim, K. Skorupski, and R. K. Taylor. PLoS Genetics. 2015

    5. Role of ToxS in the proteolytic cascade of virulence regulator ToxR in Vibrio cholerae
    S. Almagro-Moreno*, M. Z. Root, and R. K. Taylor. Molecular Microbiology. 2015

    6. Host-like carbohydrates promote bloodstream survival of Vibrio vulnificus in vivo
    J. B Lubin, W. G. Lewis, N. M. Gilbert, S. Almagro-Moreno, E. F. Boyd, A. L. Lewis. Infection and Immunity. 2015

    7. Cholera: Environmental reservoirs and impact on disease transmission
    S. Almagro-Moreno and R. K. Taylor. Microbiology Spectrum. 2013

    8. Cholera: Environmental reservoirs and impact on disease transmission
    S. Almagro-Moreno and R. K. Taylor. Book chapter for “OneHealth: People, Animals, and Environment”. ASM press. 2013

    9. Ecology and genetic structure of a northern temperate Vibrio cholerae population related to toxigenic isolates
    B. M. Schuster, A. L. Tyzik, R. A. Donner, M. J. Striplin, S. Almagro-Moreno, S. H. Jones, V. S. Cooper, and C. A. Whistler. Applied Environmental Microbiology. 2011

    10. An atomic force microscopy method for the detection of binding forces between bacteria and a lipid bilayer containing higher order gangliosides
    E. L. Adams, S. Almagro-Moreno and E. F. Boyd. Journal of Microbiological Methods. 2010

    11. Dichotomy in the evolution of pathogenicity island and bacteriophage encoded integrases from pathogenic Escherichia coli strains
    S. Almagro-Moreno, M. G. Napolitano and E. F. Boyd. Infection, Genetics and Evolution. 2010

    12. Excision dynamics of Vibrio pathogenicity island-2 from Vibrio cholerae: role of a recombination directionality factor VefA
    S. Almagro-Moreno, M. G. Napolitano and E. F. Boyd. BMC Microbiology. 2010

    13. Bacterial catabolism of nonulosonic (sialic) acid and fitness in the gut
    S. Almagro-Moreno and E. F. Boyd. Gut Microbes. 2010

    14.. How genomics has shaped our understanding of the evolution and emergence of pathogenic Vibrio cholerae
    S. Almagro-Moreno, R. Murphy, and E. F. Boyd. Book chapter for “Genomics of Foodborne and Waterborne Pathogens“. ASM press, 2010

    15. Sialic acid catabolism confers a competitive advantage to pathogenic Vibrio cholerae in the mouse intestine
    S. Almagro-Moreno and E. F. Boyd. Infection and Immunity. 2009

    16. Insights into the evolution of sialic acid catabolism among bacteria
    S. Almagro-Moreno and E. F. Boyd. BMC Evolutionary Biology. 2009

    17. Genomic islands are dynamic, ancient integrative elements in bacterial evolution
    E. F. Boyd, S. Almagro-Moreno and M. A. Parent. Trends in Microbiology. 2009

    18. The genomic code: inferring Vibrionaceae niche specialization
    F. J. Reen, S. Almagro-Moreno, D. Ussery and E. F. Boyd. Nature Reviews Microbiology.2006

     

    *Corresponding author

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    Dr. Deborah A. Altomare
  • Title: Associate Professor & Director of Transgenic Facility
  • Office: BBS 342
  • Phone: 407-266-7040
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  • Biography:

    Mechanism and treatment of pancreatic tumor progression

    The 5-year survival rate of patients diagnosed with advanced pancreatic tumor is a dismal 6% and effective therapeutic treatment strategies are needed.  The etiology leading to early stages of the disease is still unclear, although inflammation is thought to play a role. During the lag time for tumor development, there is a series of genetic alterations that is known to occur prior to rapid growth and metastasis. Our research uses genetic mouse models that have a susceptibility to develop pancreatic cancer to understand relevance to the human disease so that we can better elucidate pancreatic tumor biology, and propose preventive or therapeutic strategies for patients. Our group also has expertise in implanting human or mouse pancreatic tumor cells in the mouse pancreas so that we can test the tolerability and effectiveness of novel drug strategies to block tumor growth or metastasis.

    Preclinical response of human cancer to immune cell therapy

    Approximately 80% of ovarian cancer patients will respond to surgery and first-line chemotherapy.  However, patients frequently relapse with chemotherapy resistant disease. The challenge is to develop novel therapeutic strategies that can be effective in these patients to extend progression-free and overall survival. Different from traditional drug treatments, immune-therapeutic approaches are being investigated as a new research direction.  Our group is assessing the ability of innate immune cells, namely natural killer cells, to facilitate ovarian tumor killing.  The studies use mice implanted with human ovarian tumor cells followed by injection of human blood cells and we track response of the tumors, expansion of the immune cells, as well as persistence and homing characteristics of the immune cells in order to understand the biology and effectiveness of adoptive cell transfer as a therapy for ovarian and other cancers.

    Recent Publications

    1. Muth, A., Pandey, V., Kaur, N., Wason, M., Baker, C., Han, X., Johnson, T. R., Altomare, D.A., Phanstiel, O. IV. (2014) Synthesis and biological evaluation of antimetastatic agents predicated upon dihydromotuporamine C and its carbocyclic derivatives. J. Med. Chem. 57(10): 4023-4034.
    2. Menges, C.W., Kadariya, Y., Altomare, D.A., Talarchek, J., Neumann-Domer, E., Wu, Y., Xiao, G.-H.,  Shapiro, I., Kolev, V.N., Pachter, J.A., Klein-Szanto, A.J., Testa, J.R. (2014) Tumor suppressor alterations cooperate to drive aggressive mesotheliomas with enriched cancer stem cells via a p53-miR-34a-c-Met axis. Cancer Res. 74(4): 1261-1271.
    3. Altomare, D.A., Khaled, A.R. (2012) Homeostasis and the importance for a balance between Akt/mTOR activity and intracellular signaling. Curr. Med. Chem. 19(22): 3748-3762.
    4. Altomare, D.A., Menges, C.W., Xu, J., Pei, J., Zhang, L., Tadevosyan, A., Neumann-Domer, E., Liu, Z., Carbone, M., Chudoba, I., Klein-Szanto, A.J., Testa, J.R. (2011) Losses of both products of the Cdkn2a/Arf locus contribute to asbestos-induced mesothelioma development and cooperate to accelerate tumorigenesis. PLoS One. 6(4): e18828.
    5. Mabuchi, S., Kawase, C., Altomare, D. A., Morishige, K., Hayashi, M., Sawada, K., Ito, K., Terai, Y., Nishio, Y., Klein-Szanto, A. J., Burger, R. A., Ohmichi, M., Testa, J. R., Kimura, T. (2010) Vascular endothelial growth factor is a promising therapeutic target for the treatment of clear cell carcinoma of the ovary. Mol. Cancer Ther. 9(8): 2411-2422.
    6. Altomare, D.A., Rybak, S.M, Pei, P., Maizel. J.V., Cheung, M., Testa, J.R., Shogen, K. (2010) Onconase responsive genes in human mesothelioma cells: implications for an RNA damaging therapeutic agent. BMC Cancer. 10: 34. http://www.biomedcentral.com/1471-2407/10/34
    7. Tan, Y., You, H., Wu, C., Altomare, D.A., Testa, J.R. (2010) Appl1 is dispensable for mouse development, and loss of Appl1 has growth factor- selective effects on Akt signaling in murine embryonic fibroblasts. J. Biol. Chem. 285(9): 6377-6389.
    8. Altomare, D.A., Zhang, L., Deng, J., Di Cristofano, A., Klein-Szanto,  A.J., Kumar, R., Testa, J.R. (2010) GSK690693 delays tumor onset and progression in genetically-defined mouse models expressing activated Akt. Clin. Cancer Res. 16(2): 486-496.
    9. Mabuchi, S., Kawase, C., Altomare, D.A., Morishige, K., Sawada, K., Tsujimoto, M., Yamoto, M., Klein-Szanto, A.J., Schilder, R.J., Ohmichi, M., Testa, J.R., Kimura, T. (2009) mTOR is a promising therapeutic target both in cisplatin-sensitive and cisplatin-resistant clear cell carcinoma of the ovary. Clin. Cancer Res. 15(17): 5404-5413.
    10. Menges, C.W., Altomare, D.A., Testa, J.R. (2009) FAS-Associated Factor 1 (FAF1): diverse functions and implications for oncogenesis. Cell Cycle (Invited Perspective) 8(16): 2528-2534.
    11. Timakhov, R.A., Tan, Y., Rao, M., Lui, Z., Altomare, D.A., Xu, J., Wiest, D.L., Favorava, O.O., Knepper, J.E., Testa, J.R. (2009) Recurrent chromosomal rearrangements implicate oncogenes contributing to T-cell lymphomagenesis in Lck-MyrAkt2 transgenic mice. Genes Chromosomes Cancer, 48(9): 786-794.
    12. Altomare, D.A., Menges, C.W., Pei, J., Zhang, L., Skele-Stump, K.L., Carbone, M., Kane, A.B., Testa, J.R. (2009) Activated TNFα/NFĸB pro-survival signaling via down regulation of Fas-associated factor-1 in asbestos-induced mesotheliomas from Arf knock-out mice. Proc. Natl. Acad. Sci., USA, 106(9): 3420-3425.

    For more publication information, please visit Pubmed.

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    Chandrakala Aluganti Narasimhulu
  • Title: Assistant Scholar/Scientist
  • Office: BBS 458
  • Phone: 407.266.7120
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    Dr. Camilla Ambivero
  • Title: Assistant Professor
  • Office: HPA II 309
  • Phone: 407.823.0174
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    Sooma Ammar
  • Title: Laboratory Technician - Microprep Lab
  • Office: HPA II 344
  • Phone: 407.823.5626
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    Abby Amo-Snipes
  • Title: Purchasing Assistant
  • Office: BBS 101R
  • Phone: 407-266-7013
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    Dr. Claudia Andl
  • Title: Associate Professor
  • Office: BMS 223A
  • Phone: 407.823.1147
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  • Biography:

    Cancers of the head and neck including oral cancer are among the 10 most common cancers in the US. It is estimated that 42,440 new oral cancer cases are diagnosed in 2014. Current detection techniques often diagnose head and neck cancer as well as esophageal cancer in late stages, requiring wide local resection and radiation therapy, from which patients suffer severe disfiguration. In addition, due to limitations in early diagnostics and treatment, the 5-year survival has remained virtually unchanged over the last 30 years. The use of tobacco products, including cigarettes, cigars, pipes, and chewing tobacco, is a major risk factor together with alcohol consumption for esophageal and head and neck cancers. EndFragment

    The research interest in the Andl lab is to identify novel prognostic biomarkers and to target the signaling pathways that drive cell invasion and metastasis with focus on the tumor microenvironment.

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    Dr. Thomas Andl
  • Title: Core Scientist
  • Office: BMRA 108
  • Phone: 407.823.6542
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    Dr. Robert Borgon
  • Title: Associate Professor
  • Office: HPA II 317
  • Phone: 407-823-5798
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  • Biography:

    I teach Quantitative Biological Methods (BSC 3403), Molecular Biology I (PCB 3522), and Peer Instruction and Laboratory Occupational Training (PILOT, PCB 4943).  My prior research focused on determining the molecular structure, activation, and interactions of proteins involved in cell adhesion.

    Recent Publications

    1. Borgon RA, Verity N, Teter K.  PILOTing Undergraduate Students to Hands-On Teaching and Research Skills.  J Microbiol Biol Educ. 2013 May 6;14(1):35-46. doi: 10.1128/jmbe.v14i1.474. Print 2013.
    2. Borgon RA and Verity N.  Quantitative Biological Methods, 5th Edition.  2013.  Pearson.
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    Dr. Blaise Bossy
  • Title: Research Associate Professor
  • Office: BBS 423
  • Phone: 407.266.7141
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  • Biography:
    We are currently investigating early events in neurodegenerative diseases involving mitochondria, such as Huntington’s disease and Alzheimer’s disease. Neurons are highly dependent on mitochondria for their energy supply and their survival. These organelles are highly dynamic and can migrate, fuse or divide. During neurodegeneration, mitochondrial fragmentation occurs before neurite injury and cell death. Thus, our goal is to understand what triggers mitochondria demise. Our primary focus is the regulation of key proteins affecting mitochondrial dynamics, such as Drp1, Opa1, Mfn1 and Mfn2.
    Recent Publications
    1. Bossy, Blaise, Alejandra Petrilli, Eva Klinglmayr, Jin Chen, Ursula Lütz-Meindl, Andrew B. Knott, Eliezer Masliah, Robert Schwarzenbacher and Ella Bossy-Wetzel. S-Nitrosylation of DRP1 does not affect its enzymatic activity and is not specific to Alzheimer’s disease. J. of Alzheimer’s Disease 20: S513-S526 (2010).

    2. Liot, G., Bossy, B., Lubitz, S., Kushnareva, Y., Sejbuk, N., Bossy-Wetzel, E. Complex II inhibition by 3-NP causes mitochondrial fragmentation and neuronal cell death via an NMDA- and ROS-dependant pathway. Cell Death and Differentiation: 1-11 (2009).

    3. Song*, W., Bossy*, B., Martin*, O.J., Hicks, A., Lubitz, S., Knott, A.B., Bossy-Wetzel, E. (2008). Assessing mitochondrial morphology and dynamics using fluorescence wide-field microscopy and 3D image processing. Methods 46: 295-303 (2008). (* co-first authors).

    4. Li, H., Chen, Y., Jones, A.F., Sanger, R.H., Collis, L.P., Flannery, R., McKay, E.C., Yu, T., Schwarzenbacher, R., Bossy, B., Bossy-Wetzel, E., Bennett, M.V., Pypaert, M., Hickman, J.A., Smith, P.J., Hardwick, J.M., Jonas, E.A. (2008). Bcl-xL induces Drp-1 dependent synapse formation in cultured hippocampal neurons. Proc. Natl. Acad. Sci. USA 105(6): 2169-2174.

    5. Bossy, B., Perkins, G., Bossy-Wetzel, E. (2008) Clearing the brain’s cobweb: autophagy in neuroprotection. Current Neuropharmacology, 6(2):97-101.

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    Dr. Ella Bossy-Wetzel
  • Title: Professor
  • Office: BBS 414
  • Phone: 407.266.7139
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  • Biography:

    Dr. Bossy-Wetzel joined UCF in 2007 as tenured Professor.  She trained at Cold Spring Harbor Laboratory and the University of California, San Francisco and the Pasteur Institute of Paris, France.  Prior to joining UCF, Dr. Bossy-Wetzel was an Assistant Professor at the Burnham Institute for Medical Research in La Jolla, California.  She has received numerous prestigious awards from organizations including the Human Frontier Science Program Organization, the European Molecular Biology Organization, Swiss National Funds, National Institutes of Health, the American Parkinson’s Disease Foundation, and the Hereditary Disease Foundation.  Her laboratory is currently funded by a grant from the National Institute for Neurological Disease and Stroke.  Her publications have received over 14100 citations with an h-index of 40. She serves yearly on numerous grant review boards for the National Institutes of Health, the National Science Foundation, and the Swiss National Funds.

    MISSION

    The mission of our laboratory is to identify the critical events that cause neurodegeneration. Our ultimate goal is to improve the lives of patients and their families by developing effective treatments that can cure or prevent neurodegenerative diseases.

    CHALLENGE

    While physicians can recognize and identify the clinical symptoms of most neurodegenerative disorders, current treatments merely treat the symptoms and cannot cure the disease. Therefore, new discoveries are urgently needed that will lead to therapies that can prevent the relentless and progressive neuronal loss. Our laboratory addresses this challenge by identifying the key events that cause neurodegeneration. We are working on hereditary and sporadic disorders including Alzheimer’s disease, Huntington’s disease, Amyotrophic Lateral Sclerosis, and Optic Atrophy. We focus on mitochondria primarily, because mitochondrial injury is an early and central event in many if not all neurodegenerative diseases, and thus represents an opportunity for therapeutic intervention.

    APPROACH

    To embark on this challenge and to map the key events that push neurons into degenerative cascades, we have developed sophisticated, quantitative time-lapse imaging techniques. We use these systems to decipher the temporal and spatial sequence of events related to neurodegeneration in living neurons, and to test potential therapeutic agents that may interfere with this process. In addition to primary neurons our laboratory uses mouse models of neurodegeneration and human patient samples. Our approach is interdisciplinary and includes cell biology, biochemistry, genetics, biophysics, electron microscopy, and structure biology.

    MITOCHONDRIA IN NEURONS

    Mitochondria in nerve cells are crucial for energy supply and the maintenance of effective communication networks between neurons, needed for learning and memory. The body uses twenty percent of its energy to maintain normal brain function. Mitochondria must supply most of this energy. Thus, it comes as no surprise that mitochondrial injury can have devastating effects on the brain and nervous system. Mitochondria also serve as sinks for calcium ions that accumulate after neuronal firing and neurotransmission. Additionally, injured mitochondria act as reactors. Similar to damaged power plants, they can leak hazardous materials such as cytochrome c or free radicals that can ignite subsequent nerve cell injury and, ultimately, result in neuronal death.  To meet the intense energy requirements, each neuron has several hundred mitochondria. Mitochondria in healthy neurons resemble long filaments, equally spaced along nerve processes similar to train tracks, permitting effective energy transmission across extreme distances that can reach a meter in motor neuron axons. Besides their often cable-like morphology, mitochondria in neurons are remarkably dynamic, traveling along nerve processes and undergoing cycles of mitochondrial fission and fusion.

    MITOCHONDRIAL FISSION AND FUSION

    A conserved battery of large dynamin-related GTPases with opposing functions orchestrates mitochondrial fission and fusion. Dynamin-related protein 1 (Drp1) regulates mitochondrial fission and Mitofusin-1 and -2 (Mfn1,2) and Optic Atrophy 1 (OPA1) mediate mitochondrial fusion. Interestingly, patients suffering of the neurodegenerative disorders Charcot-Marie-Tooth syndrome type 2A, a peripheral neuropathy, and dominant optic atrophy, an optic neuropathy, carry mutations in Mfn2 and OPA1, respectively. These findings underscore the importance of mitochondrial fusion in neuronal function and suggest that tilting the balance of mitochondrial fission and fusion toward continuous fission can set off a neurodegenerative cascade. Mitochondrial fusion may protect neurons by preventing depletion of metabolites or mitochondrial DNA. Without fusion deficiencies may become manifest, thus leading to a vicious cycle.

    MITOCHONDRIAL FRAGMENTATION IN NEURODEGENERATION

    During brain injury neurons release glutamate, an excitatory neurotransmitter that causes excessive activation of glutamate receptors of the NMDA subtype. Activation of NMDA receptors leads to rapid calcium influx and nitric oxide (NO) accumulation. Too much NO can combine with superoxide anions to form highly neurotoxic peroxynitrite. We recently discovered that NO triggers profound mitochondrial fission accompanied by ultrastructural changes of mitochondria, autophagy, ATP decline, and free radical production. Blocking mitochondrial fission and increasing mitochondrial fusion delayed neuronal cell death. Our results suggest that mitochondrial fission occurs early and contributes to ischemic stroke and the pathogenesis of Alzheimer’s disease, Huntington’s disease, Parkinson’s disease, optic nerve damage, and motor neuron disease including ALS.

    Recent Publications

    1. Loss of OPA1 disturbs cellular calcium homeostasis and sensitizes for excitotoxicity. Kushnareva YE, Gerencser AA, Bossy B, Ju WK, White AD, Waggoner J, Ellisman MH, Perkins G, Bossy-Wetzel E. Cell Death Differ. 2012 Nov. 9
    2. Purification, crystallization and X-ray diffraction analysis of human dynamin-related protein 1 GTPase-GED fusion protein. Klinglmayr E, Wenger J, Mayr S, Bossy-Wetzel E, Puehringer S. Acta Crystallogr. Sect F Struct Biol Cyrst Commun. 2012 Oct.1; 68: 1217-21.
    3. Mutant SOD1 (G93A) triggers mitochondrial fragmentation in spinal cord motor neurons: Neuroprotection by SIRT3 and PGC-1a. Song W, Song Y, Kincaid B, Bossy B, Bossy-Wetzel E. Neurobiol Dis 2012 Jul. 20
    4. Mutant huntingtin binds the mitochondrial fission GTPase dynamin-related protein-1 and increases its enzymatic activity. Song W, Chen J, Petrilli A, Liot G, Klinglmayr E, Zhou Y, Poquiz P, Tjong J, Pouladi MA, Hayden MR, Masliah E, Ellisman M, Rouiller I, Schwarzenbacher R, Bossy B, Perkins G, Bossy-Wetzel E.Nat Med. 2011 Feb 20.
    5. Impact of nitric oxide on metabolism in health and age-related disease. Knott AB,Bossy-Wetzel E. Diabetes Obes Metab. 2010 Oct;12 Suppl 2:126-33.
    6. Membrane remodeling induced by the dynamin-related protein Drp1 stimulates Bax oligomerization. Montessuit S, Somasekharan SP, Terrones O, Lucken-Ardjomande S, Herzig S, Schwarzenbacher R, Manstein DJ, Bossy-Wetzel E, Basañez G, Meda P, Martinou JC. Cell. 2010 Sep 17;142(6):889-901.
    7. S-Nitrosylation of DRP1 does not affect enzymatic activity and is not specific to Alzheimer’s disease. Bossy B, Petrilli A, Klinglmayr E, Chen J, Lütz-Meindl U, Knott AB, Masliah E, Schwarzenbacher R, Bossy-Wetzel E.J Alzheimers Dis. 2010;20 Suppl 2:S513-26.
    8. New insights into mitochondrial structure during cell death.Perkins G, Bossy-Wetzel E, Ellisman MH. Exp Neurol. 2009 Aug;218(2):183-92. Epub 2009 May 21. Review.
    9. Clearing the brain’s cobwebs: the role of autophagy in neuroprotection.Bossy B, Perkins G, Bossy-Wetzel E.Curr Neuropharmacol. 2008 Jun;6(2):97-101.
    10. Complex II inhibition by 3-NP causes mitochondrial fragmentation and neuronal cell death via an NMDA- and ROS-dependent pathway. Liot G, Bossy B, Lubitz S, Kushnareva Y, Sejbuk N, Bossy-Wetzel E. Cell Death Differ. 2009 Jun;16(6):899-909. Epub 2009 Mar 20.
    11. Impairing the mitochondrial fission and fusion balance: a new mechanism of neurodegeneration. Knott AB, Bossy-Wetzel E.Ann N Y Acad Sci. 2008 Dec;1147:283-92. Review.
    12. Assessing mitochondrial outer membrane permeabilization during apoptosis.Dave Z, Byfield M, Bossy-Wetzel E. Methods. 2008 Dec;46(4):319-23. Epub 2008 Oct 26.
    13. Assessing mitochondrial morphology and dynamics using fluorescence wide-field microscopy and 3D image processing. Song W, Bossy B, Martin OJ, Hicks A, Lubitz S, Knott AB, Bossy-Wetzel E. Methods. 2008 Dec;46(4):295-303. Epub 2008 Oct 24.
    14. Mutant huntingtin and mitochondrial dysfunction. Bossy-Wetzel E, Petrilli A, Knott AB. Trends Neurosci. 2008 Dec;31(12):609-16. Epub 2008 Oct 24. Review.
    15. Nitric oxide in health and disease of the nervous system. Knott AB, Bossy-Wetzel E.Antioxid Redox Signal. 2009 Mar;11(3):541-54. Review.
    16. Mitochondrial fragmentation in neurodegeneration. Knott AB, Perkins G, Schwarzenbacher R, Bossy-Wetzel E. Nat Rev Neurosci. 2008 Jul;9(7):505-18. Review.
    17. Mitochondrial swelling measurement in situ by optimized spatial filtering: astrocyte-neuron differences. Gerencser AA, Doczi J, Töröcsik B, Bossy-Wetzel E, Adam-Vizi V.Biophys J. 2008 Sep;95(5):2583-98. Epub 2008 Apr 18.
    18. Bcl-xL induces Drp1-dependent synapse formation in cultured hippocampal neurons. Li H, Chen Y, Jones AF, Sanger RH, Collis LP, Flannery R, McNay EC, Yu T, Schwarzenbacher R, Bossy B, Bossy-Wetzel E, Bennett MV, Pypaert M, Hickman JA, Smith PJ, Hardwick JM, Jonas EA. Proc Natl Acad Sci U S A. 2008 Feb 12;105(6):2169-74. Epub 2008 Feb 4.
    19. A Golgi fragmentation pathway in neurodegeneration.Nakagomi S, Barsoum MJ,Bossy-Wetzel E, Sütterlin C, Malhotra V, Lipton SA. Neurobiol Dis. 2008 Feb;29(2):221-31. Epub 2007 Sep 7.
    20. ALS: astrocytes take center stage, but must they share the spotlight? Knott AB,Bossy-Wetzel E.Cell Death Differ. 2007 Dec;14(12):1985-8. Epub 2007 Oct 5. No abstract available
    21. Mitochondrial fission is an upstream and required event for bax foci formation in response to nitric oxide in cortical neurons. Yuan H, Gerencser AA, Liot G, Lipton SA, Ellisman M, Perkins GA, Bossy-Wetzel E.Cell Death Differ. 2007 Mar;14(3):462-71. Epub 2006 Oct 20

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    Dr. Emily Bradshaw
  • Title: Assistant Professor
  • Office: HPAII 311
  • Phone: 407.823.4919
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    Dr. Debopam Chakrabarti
  • Title: Professor & Molecular Microbiology Division Leader
  • Office: Biomedical Research Annex (BRA) 140
  • Phone: 407.882.2256
  • Send an Email
  • Biography:

    Malaria afflicts about half of the world population causing over 500,000 deaths each year. In addition to contributing significantly towards overall childhood mortality in the poorest nations, the disease is estimated to cause considerable reductions in the economic growth of countries that bear a heavy malaria burden. The situation is made worse because the widespread prevalence of drug resistant parasites is rendering the limited number of available drugs less and less effective for clinical use. Therefore, there is a pressing need for novel therapeutic options to treat multidrug resistant malaria. It is also important to understand the molecular mechanism of parasite growth and differentiation so that novel therapeutic targets can be identified.

    A major focus of research in my laboratory is to identify next generation of antimalarial compounds from unique areas of medicinally relevant chemical space. To pursue this goal we are engaged in screening focused libraries of natural product-based synthetic compounds as well as natural product extracts from under explored marine biodiversity and fungi.  Our research has discovered many novel scaffolds with potent and selective antiplasmodial activities with cellular action distinct from current antimalarials, including one that cures malaria in the rodent model. Another aspect of research in my laboratory focuses on understanding molecular mechanisms of the intraerythrocytic life cycle of the malaria parasite, Plasmodium falciparum. Specifically, we are engaged in defining precise physiological roles of Plasmodium protein kinases that are key regulators of its complex developmental stages through identification of their substrates. We recently performed isobaric tag-based quantitative proteomics and phosphoproteomics analyses of three developmental stages in the Plasmodium asexual cycle. Our system-wide comprehensive analysis is a major step towards elucidation of kinase-substrate pairs operative in various signaling networks in the parasite. This rich dataset will be useful in defining and targeting the parasite’s signaling network. Many of the unique features of parasite protein kinases can potentially be exploited to design new generation of malaria therapeutics.

    Recent Publications

    1. Roberts, B.F., Iyamu, I.D., Lee, S., Lee, E., Ayong, L., Kyle, D.E., Yuan, Y., Manetsch, R., Chakrabarti, D. (2016) Spirocyclic chromanes exhibit antiplasmodial activities and inhibit all intraerythrocytic life cycle stages. Int. J. Parasitol. Drugs Drug Resist. 6, 85-92.
    2. Chakrabarti, D. and Wright, A. (2015) Anti-malarial compounds from marine natural compounds. US Patent: 9,181,251 B2. Nov 10, 2015.
    3. Arora, S., Mauser, J., Chakrabarti, D., Schulte, A. (2015) Spatially resolved micro-absorption spectroscopy with a broadband source and confocal detection. Optics Communication, 355, 533-537.
    4. Koyama, F.C., Azevedo, M.F., Budu, A., Chakrabarti, D., Garcia, C.R. (2014) Melatonin-induced upregulation of gene expression related to ubiquitin/proteasome system in human malaria parasite Plasmodium falciparum. Int. J. Mol. Sci. 15, 22320-30.
    5. Pease, B., Huttlin, E., Jedrychowski, M.P., Talevich, E., Harmon, J., Dillman, T., Kannan, N., Doerig, C., Chakrabarti, R., Gygi, S., Chakrabarti, D. (2013) Global analysis of protein expression and phosphorylation of three stages of Plasmodium falciparum intraerythrocytic development. J. Proteome. Res. 12, 4028-45.
    6. Alvarado, S. Roberts, BF, Wright, A.E., Chakrabarti, D. (2013) The bis(indolyl)imidazole alkaloid nortopsentin A exhibits antiplasmodial activity. Antimicrob Agents Chemother 57, 2362-64.
    7. Dorin-Semblat, D., Carvalho, T. G., Nivez, M-P.,Goldring, D., Chakrabarti, D., Dhar, S., Goldberg, D., Tilley, L., Doerig, C. (2013) An atypical cyclin-dependent kinase controls Plasmodium falciparum proliferation rate. Kinome 1, 4-16.
    8. Koyama, F.C., Ribiero, R.Y., Garcia, J.L. Chakrabarti, D., and Garcia, C.R. (2012) Ubiquitin proteasome system and the atypical kinase PfPK7 are involved in melatonin signaling in Plasmodium falciparum . J. Pineal Res. 53, 147-53.
    9. Dorin-Semblat, D., Goldring, D., Patterson, S., Quashie, N., Reininger, L., Schmitt, S., Meijer, L., Chakrabarti, D., and Doerig, C. (2011) Plasmodium falciparum NIMA-related kinase Pfnek-1: sex-specificity, essentiality for the erythrocytic asexual cycle. Microbiology 157, 2785-94.
    10. Ayong, L., Da Silva, T., Mauser, J., Allen, C.A., Chakrabarti, D. (2011) Evidence for prenylation-dependent targeting of a Ykt6 SNARE in Plasmodium falciparum. Mol. Biochem. Parasitol. 175, 162-8.
    11. Halbert, J., Ayong, L., Equinet, L., Le Roch, K., Hardy, M., Goldring, D., Chakrabarti, D., Reininger, L., Doerig, C. (2010) A Plasmodium falciparum transcriptional cyclin-dependent kinase-related kinase with a crucial role in parasite proliferation associates with histone deacytylase activity. Eukaryot. Cell 9, 952-9.
    12. Davoodi-Semiromi A., Schreiber, M., Nalapalli, S., Verma, D., Singh, N. D, Banks, R. K., Chakrabarti, D., Daniell, H. (2010) Chloroplast-derived vaccine antigens confer dual immunity against cholera and malaria by oral and injectable delivery. Plant Biotechnol. J., 8, 223-48.
    13. Ayong, L., Raghavan, A., Schneider, T.G., Taraschi, T. F., Fidock, D. A., Chakrabarti, D. (2009). The longin domain regulates the steady state dynamics of Sec 22 in Plasmodium falciparum. Eukaryot. Cell, 8, 1330-40.
    14. Koyama, F.C., Chakrabarti, D., Garcia C. R. (2009) Molecular Machinery of signal transduction and cell cycle regulation in Plasmodium. Mol. Biochem. Parasitol. 165, 1-7.
    15. Chakrabarti, D. (2009). A methods-based biotechnology course for undergraduates. Biochem. Mol. Biol. Educ. 37, 227-31.
    16. Chakrabarti, R., Chakrabarti, D. (2009) Chemotherapeutics of neglected waterbourne parasites: current status and future perspectives. Mol. Cell. Pharmacol. 1, 98-102.

     

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    Dr. Ratna Chakrabarti
  • Title: Associate Professor
  • Office: Biomedical Research Annex (BRA) 140
  • Phone: 407.882.2258
  • Send an Email
  • Biography:

    Research in my laboratory is focused toward understanding the molecular mechanism of regulation of gene expression in prostate and breast cancer, specifically, components of signaling pathways that are involved in cell cycle regulation, progression of metastasis and development of drug resistance. One of the major challenges for treatment of aggressive prostate cancer is development of resistance to chemotherapeutic agents and hormone ablation therapy. We are conducting research on the role of microRNAs on regulation of gene expression and development of resistance to therapies. Our research led to identification of a signature set of microRNAs for detection of aggressive and drug resistant cancers.  Additionally, we are determining the mechanism of altered responsiveness to the agents that are involved in induction of mitotic arrest and apoptosis. Our research is directed towards determining the functional roles of cell cycle regulatory proteins, kinases and proteinases on cell cycle progression and turnover of tumor microenvironment. Our studies indicated that DNA replication licensing protein Cdc6 is hormonally regulated and its expression profile could be used as a diagnostic marker for progression and metastasis of prostate cancer. Our studies also identified a functional link between expression of a cytoskeleton regulatory protein and promotion of invasion and metastasis. We are also conducting high throughput screening of compound libraries for identifying novel anticancer agents. Furthermore, we are conducting collaborative research on optimization of uniquely fabricated multifunctional biodegradable polymer particles for cell-specific binding and delivery of therapeutics specifically to cancer cells, and separation of cancer cells from normal cells. Our collaborative research also includes studies on the function of kinases and their native substrates in regulation of cell cycle progression through reversible protein phosphorylation in protozoan parasites.

    Recent Publications

    1. Ritchey, L. and Chakrabarti. R. (2014) Aurora A kinase modulates actin cytoskeleton through phosphorylation of Cofilin: Implication in the mitotic process. Biochem Byophys Acta, 1843: 2719-2729.
    2. Ottman, R, Nguyen, C., Lorch, R., Chakrabarti, R. (2014).  MicroRNA expressions associated with progression of prostate cancer cells to antiandrogen therapy resistance. Mol. Cancer.13:1
    3. Pease, B., Huttlin, E., Jedrychowski, M.P., Talevich, E., Harmon, J., Dillman, T., Kannan, N.,  Doerig, C., Chakrabarti, R., Gygi, S., Chakrabarti, D. (2013) Global analysis of protein expression phosphorylation of three stages of Plasmodium falciparum Intraerythrocytic development. J. Proteome. Res. 12:4028-45
    4. Kaufman, J., Ottman, R., Tao, G., Shabahang, S., Banaei, E., Liang, X., Johnson, S.G., Fink, Y., Chakrabarti, R. And Abouraddy, A.F. (2013). In-fiber emulsification of polymer particles for biosensing and encapsulation. Proc. Natl. Acad. Sci. 110:15549-54
    5. Ritchey, L., Ottman, R., Roumanos, M and Chakrabarti, R. (2012). A functional cooperativity between Aurora A kinase and LIM kinase1: Implication in the mitotic process Cell Cycle, 11:296-309.
    6. Tapia, T., Ottman, R.  and Chakrabarti, R. (2011). LIM kinase1 modulates function of membrane type matrix metalloproteinase 1: implication in invasion of prostate cancer cells. Mol. Cancer, 10:6.
    7. Illegbushi, O.J., Song, H. and Chakrabarti, R. (2010). Biocompatibility and conductometric property of Sol-Gel derived ZnO/PVP nanocomposite biosensor film. J. Bion. Eng. 7, suppl. S-30-S-35. future perspectives. Mol. Cell. Pharmacol. 1: 98-102.
    8. Chakrabarti, R. (2010). LIMK1 (LIMK domain kinase1) Atlas Genet. Cytogenet. Oncol. Haematol. 2010; 14:641-644.
    9. Ghosh, D. and Chakrabarti, R (2009). Joint variable selection and classification with immunohistochemical data. Biomarker Insights, 4: 103-110.
    10. Chakrabarti, R and Chakrabarti, D. (2009). Chemotherapeutics of neglected waterborne parasites: current status and future perspectives. Mol. Cell. Pharmacol. 1: 98-102.

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    Dr. Li-Mei Chen
  • Title: Research Associate Professor & BMS Core Manager
  • Office: BMS 324
  • Phone: 407.823.3585
  • Send an Email
  • Biography:

    We are investigating the impact of cigarette smoking on human health. Cigarette smoke compromises lung epithelium integrity and causes lung inflammation, which eventually leads to chronic lung diseases such as emphysema and bronchitis. It has been known for many years that chronic inflammation is associated with epithelial carcinogenesis. Smokers with airway inflammation have a higher risk of lung cancer compared with smokers without chronic inflammation. Targeting the inflammatory mediators has been investigated as a therapeutic strategy for decreasing the incidence and spread of cancers. Prostasin is an epithelial glycosylphosphatidylinositol-anchored membrane serine protease. Prostasin has been implicated for mechanistic roles in maintaining the integrity of the epithelium via regulating the tight junctions at the cell-cell contacts, in taming innate epithelial inflammation via attenuating the expression of inducible nitric oxide synthase, and in inhibiting tumor cell invasion and metastasis. Our research is focused on elucidating the mechanisms of prostasin’s roles during inflammation and cancer development and progression.

    Recent Publications

    1. Chen L-M, Chang M, Dai Y, Chai KX, Dyrskjøt L, Sanchez-Cabayo M, Szarvas T, Zwarthoff EC, Lokeswhar V, Jeronimo C, Parker AS, Ross S, Borre M, Orntoft TF, Jaeger T, Beukers W, Lopez LE, Henrique R, Young PR, Urquidi V, Goodison S, Rosser CJ. (2014) External Validation of a Multiplex Urinary Protein Panel for the Detection of Bladder Cancer in a Multicenter Cohort. Cancer Epidemiol Biomarkers Prev. Jun 11 [Epub ahead of print]
    2. Wood MP, Cole AL, Eade CR, Chen L-M, Chai KX, Cole AM. (2014) The HIV-1 gp41 ectodomain is cleaved by matriptase to produce a chemotactic peptide that acts through FPR2. Immunology 142(3):474-83.
    3. Chen L-M, Nergard JC, Ni L, Rosser CJ, Chai KX. (2013) Long-term exposure to cigarette smoke extract induces hypomethylation at the RUNX3 and IGF2-H19 loci in immortalized human urothelial cells. PLoS One 8(5):e65513.
    4. Fu YY, Nergard JC, Barnette NK, Wang YL, Chai KX, and Chen L-M. (2012) Effect of cigarette smoke extract on the expression of granulocyte-macrophage colony-stimulating factor expression in a normal human trophoblast cell line. PLoS One 7(8):e43042.
    5. Xu Z, Chen YW, Battu A, Wilder P, Weber D, Yu W, Mackerell AD, Chen L-M, Chai KX, Johnson MD, Lin CY. (2011). Targeting zymogen activation to control the matriptase-prostasin proteolytic cascade. J Med Chem 2011 Nov 10;54(21):7567-78. Epub 2011 Oct 12. PMID: 21966950
    6. Martellini JA, Cole AL, Svoboda P, Stuchlik O, Chen L-M, Chai KX, Gangrade BK, Sørensen OE, Pohl J, Cole AM (2011). HIV-1 Enhancing effect of prostatic acid phosphatase peptides is reduced in human seminal plasma. PLoS One 6(1):e16285.
    7. Chen YW, Chou FP, Chen CY, Rorke EA, Wang JK, Chen L-M, Chai KX, Eckert RL, Johnson MD, and Lin CY. (2010). Regulation of the matriptase-prostasin cell surface proteolytic cascade by hepatocyte growth factor activator inhibitor-1 during epidermal differentiation. J Biol Chem 285(41):31755-62.
    8. Gao L, Smith RS, Chen L-M, Chai KX, Chao L. Chao J. (2010) Tissue kallikrein promotes prostate cancer cell migration and invasion via a protease-activated receptor-1-dependent signaling pathway. Biol Chem. 391(7):803-12.
    9. Wang C, Ma L, Chen L-M, Chai KX, and Su M. (2010) Scanning calorimetric detections of multiple DNA biomarkers contained in complex fluids. Anal Chem. 82(5):1838-43.
    10. Fu YY, Gao WL, Chen M, Chai KX, Wang YL, and Chen L-M. (2010) Prostasin regulates human placental trophoblast cell proliferation via the epidermal growth factor receptor signaling pathway. Hum Reprod. 25(3):623-32.
    11. Chen M, Chen L-M, Lin CY, and Chai KX. (2010) Hepsin activates prostasin and cleaves the extracellular domain of the epidermal growth factor receptor. Mol. Cell. Biochem. 337(1-2):259-66.
    12. Chen L-M, Verity NJ, and Chai KX. (2009) Loss of prostasin (PRSS8) in human bladder transitional cell carcinoma cell lines is associated with epithelial-mesenchymal transition (EMT). BMC Cancer. 9:377.
    13. Ma XJ, Fu YY, Li YX, Chen L-M, Chai KX, Wang YL. (2009) Prostasin inhibits cell invasion in human choriocarcinomal JEG-3 cells. Histochem. Cell Biol. 132(6):639-46.
    14. Chen L-M, Hatfield ML, Fu YY, and Chai KX. (2009) Prostasin regulates iNOS and cyclin D1 expression by modulating protease-activated receptor-2 signaling in prostate epithelial cells. Prostate 69(16):1790-801.

    Book Chapters

    1. Chao J, Chen L-M, Chai KX. (2013) Prostasin. In The Handbook of Proteolytic Enzymes, 3rd edition. Edited by: Rawlings, N.D. and Guy, S. Elsevier., pp3011-3014
    2. Chao J, Chen L-M, Chai KX. (2013) Human kallikrein-related peptidase 2. In The Handbook of Proteolytic Enzymes, 3rd edition. Edited by: Rawlings, N.D. and Guy, S. Elsevier., pp2762-2765
    3. Chao J, Chai KX, Chen L-M. (2013) Human kallikrein-related peptidase 3, the prostate-specific antigen. In The Handbook of Proteolytic Enzymes, 3rd edition. Edited by: Rawlings, N.D. and Guy, S. Elsevier., pp2765-2768
    4. Chen L-M, Chai KX. (2012) PRSS8 (protease, serine, 8). Atlas Genet Cytogenet Oncol Haematol. 16(9):658-664.
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    Dr. Zixi (Jack) Cheng
  • Title: Associate Professor
  • Office: BMS 230
  • Phone: 407.823.1505
  • Send an Email
  • Biography:

    Cardiovascular diseases are the leading cause of mortality and morbidity and many of the cardiovascular disorders (hypertension, cardiomyopathy, decreased cardiac reflexes, and cardiac failure) are intimately associated with aging, sleep apnea (intermittent hypoxia), and diabetes mellitus. Among these disorders, the reduction of autonomic control of the heart rate in patients is very dangerous and it is commonly used as a risk predictor for life threatening arrhythmia which causes sudden death. However, the neural mechanisms involved in cardiac neuropathy of aging, intermittent hypoxia, and diabetes-related cardiovascular morbidity, are poorly understood.  More specifically, precise physiological and anatomical assessments of reductions in autonomic control of the cardiovascular function and the underlying morphological reorganization of cardiac circuitry during aging, following intermittent hypoxia (sleep apnea), in chronic diabetes are currently poorly defined due to past technical limitations. Detailed characterization of the organization and reorganization of autonomic axons and terminals in cardiac tissues is an essential component towards increasing our understanding of aging-, chronic intermittent hypoxia-, and diabetes- related cardiac processes. The long-term goal of my research is first to study modifications of the cardiac functions and the changes of the neural circuitry in the brain-heart axis of aged, intermittent hypoxia-exposed, and diabetes in rat and mouse models at different ages (young, mid-age, and old) as well as to characterize cardiac nerve regeneration after denervation. Then, we will seek for medical interventions to prevent/reduce such pathological changes as well as to promote cardiac nerve regeneration.

    We will use the recent technological advances in my lab and my collaborators’ labs to test our leading hypothesis that functional changes, morphological reorganization, and enhanced ROS production of the parasympathetic nervous system occur at multiple sites within the brain-heart axis in intermittent hypoxia-exposed and chronic diabetic animals. Since advanced age is a strong risk factor for neuropathy, we further hypothesize that aging and diabetes/sleep apnea may interact to exacerbate deleterious processes.

    Technically, we have first successfully developed a combination of novel anatomical techniques, including microinjections, anterograde tracing, laser scanning confocal microscopy, and stereological counting strategies to qualitatively and quantitatively characterize vagal cardiac axons and terminals in rat hearts. Second, we have established a selective lesion protocol to dissect the functional roles of nucleus ambiguus (NA) and the dorsal motor nucleus of the vagus (DmnX). Thirdly, we have obtained a unique transgenic mouse model of chronic type 1 diabetes (OVE26), thereby permitting detailed examination of functional and anatomical alterations in the chronic diabetic heart. Fourth, we have used a rather unique rodent model of intermittent hypoxia that closely mimics the behavioral, anatomical, and physiological consequences of obstructive sleep apnea. Therefore, we are able to examine the functional and anatomical alterations in chemoreceptor and baroreceptor reflexes.  Finally, we have established two physiological systems which will allow us to record aortic nerve activity in vivo and to patch-clamp baroreceptor neurons in the nodose ganglion of rats.

    Recent Publications

     

    1: Cheng ZJ. Vagal cardiac efferent innervation in F344 rats: Effects of chronic

    intermittent hypoxia. Auton Neurosci. 2016 Oct 29. pii: S1566-0702(16)30236-3.

    doi: 10.1016/j.autneu.2016.10.005. [Epub ahead of print] PubMed PMID: 27839717.

     

     

    2: Hatcher J, Gu H, Cheng ZJ. SOD1 Overexpression Preserves Baroreflex Control of

    Heart Rate with an Increase of Aortic Depressor Nerve Function. Oxid Med Cell

    Longev. 2016;2016:3686829. doi: 10.1155/2016/3686829. PubMed PMID: 26823951;

    PubMed Central PMCID: PMC4707341.

     

     

    3: Harris DM, Bellew C, Cheng ZJ, Cendán JC, Kibble JD. High-fidelity patient

    simulators to expose undergraduate students to the clinical relevance of

    physiology concepts. Adv Physiol Educ. 2014 Dec;38(4):372-5. doi:

    10.1152/advan.00063.2014. PubMed PMID: 25434023.

     

     

    4: Li L, Hatcher JT, Hoover DB, Gu H, Wurster RD, Cheng ZJ. Distribution and

    morphology of calcitonin gene-related peptide and substance P immunoreactive

    axons in the whole-mount atria of mice. Auton Neurosci. 2014 Apr;181:37-48. doi:

    10.1016/j.autneu.2013.12.010. PubMed PMID: 24433968.

     

    1. Gui L, Bao Z, Jia Y, Qin X, Cheng ZJ, Zhu J, Chen QH. Ventricular

    tachyarrhythmias in rats with acute myocardial infarction involves activation of

    small-conductance Ca2+-activated K+ channels. Am J Physiol Heart Circ Physiol.

    2013 Jan 1;304(1):H118-30. doi: 10.1152/ajpheart.00820.2011. PubMed PMID:

    23086994.

     

    6: Dayyat EA, Zhang SX, Wang Y, Cheng ZJ, Gozal D. Exogenous erythropoietin

    administration attenuates intermittent hypoxia-induced cognitive deficits in a

    murine model of sleep apnea. BMC Neurosci. 2012 Jul 3;13:77. doi:

    10.1186/1471-2202-13-77. PubMed PMID: 22759774; PubMed Central PMCID: PMC3412695.

     

     

     

    7: Lin M, Hatcher JT, Wurster RD, Chen QH, Cheng ZJ. Characteristics of single

    large-conductance Ca2+-activated K+ channels and their regulation of action

    potentials and excitability in parasympathetic cardiac motoneurons in the nucleus

    ambiguus. Am J Physiol Cell Physiol. 2014 Jan 15;306(2):C152-66. doi:

    10.1152/ajpcell.00423.2012. PubMed PMID: 24196530; PubMed Central PMCID:

    PMC3919986.

     

     

    8: Lin M, Hatcher JT, Chen QH, Wurster RD, Li L, Cheng ZJ. Maternal diabetes

    increases large conductance Ca2+-activated K+ outward currents that alter action

    potential properties but do not contribute to attenuated excitability of

    parasympathetic cardiac motoneurons in the nucleus ambiguus of neonatal mice. Am

    J Physiol Regul Integr Comp Physiol. 2011 May;300(5):R1070-8. doi:

    10.1152/ajpregu.00470.2010. PubMed PMID: 21248308; PubMed Central PMCID:

    PMC3094040.

     

     

    9: Lin M, Hatcher JT, Chen QH, Wurster RD, Cheng ZJ. Small conductance

    Ca2+-activated K+ channels regulate firing properties and excitability in

    parasympathetic cardiac motoneurons in the nucleus ambiguus. Am J Physiol Cell

    Physiol. 2010 Dec;299(6):C1285-98. doi: 10.1152/ajpcell.00134.2010. PubMed PMID:

    20739619; PubMed Central PMCID: PMC3774095.

     

     

    10: Lin M, Chen QH, Wurster RD, Hatcher JT, Liu YQ, Li L, Harden SW, Cheng ZJ.

    Maternal diabetes increases small conductance Ca2+-activated K+ (SK) currents

    that alter action potential properties and excitability of cardiac motoneurons in

    the nucleus ambiguus. J Neurophysiol. 2010 Oct;104(4):2125-38. doi:

    10.1152/jn.00671.2009. PubMed PMID: 20668269; PubMed Central PMCID: PMC2957455.

     

    For more publication information, please visit Pubmed.

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    Dr. Alexander M. Cole
  • Title: Professor
  • Office: BMS 236A
  • Phone: 407.823.3633
  • Send an Email
  • Biography:

    For the past two decades, Dr. Cole has been investigating an increasingly important aspect of the human immune system called “innate host defense”, which is involved in the body’s immediate response to germs such as viruses and bacteria. The main pathogenic virus that he studies is HIV (human immunodeficiency virus), which can cause the disease AIDS (acquired immunodeficiency syndrome). Worldwide, the majority of new HIV infections are in women who contracted the virus through sexual contact, which has prompted Dr. Cole to study women’s health aspects that lead to HIV transmission. Additionally, his lab is interested in developing prophylactic drugs called “microbicides” that can prevent or limit sexually transmitted HIV. A new microbicide that his lab has developed is currently being tested to confirm that it is safe and effective against HIV.

    Dr. Cole also studies how the bacterium Staphylococcus aureus, or “Staph”, can colonize the inside of human noses and be transmitted to other people. While Staph is essentially harmless to a person’s nose, that nose serves as a major reservoir for transmitting Staph and causing serious disease. Since this bacterium alone accounts for more deaths in the U.S. than HIV/AIDS, and many Staph are resistant to the majority of available antibiotics, it is evermore important to understand how humans can harbor this bacterium in their noses and to develop new drugs to kill Staph. Both of these aspects are being actively pursued in Dr. Cole’s laboratory.

    Recent Publications

    1. Sivaraman, K., A.M. Cole. (2009). Pathogenesis gene families in the common minimal genome of Staphylococcus aureus are hypervariable. FEBS Letters. 583(8): 1304-8. (PMCID: PMC2677416)
    2. Martellini, J.A., A.L. Cole, N. Venkataraman, G.A. Quinn, P. Svoboda, B.K. Gangrade, J. Pohl, O.E. Sørensen, and A.M. Cole. (2009). Cationic polypeptides are major anti-HIV-1 factors in human seminal plasma. FASEB J. 23(10): 3609-18. NIHMS# 219133
    3. Quinn, G.A., P.M. Tarwater, and A.M. Cole. (2009). Subversion of IL-1-mediated host defense by a nasal carrier strain of Staphylococcus aureus. Immunology. 128: e222-229. (PMCID:  PMC2753939)
    4. Venkataraman, N., A.L. Cole, P. Ruchula, A.J. Waring, R.I. Lehrer, O. Stuchlik, J. Pohl, and A.M. Cole. (2009). Reawakening retrocyclins:  ancestral human theta-defensins with activity against HIV-1. PLoS Biology. 7(4): e95. (PMCID: PMC2672613). (received Editor’s pick, and was selected for a commissioned synopsis)
    5. Cole, A.M., D.L. Patton, L.C. Rohan, A.L. Cole, Y. Cosgrove-Sweeney, N.A. Rogers, D. Ratner, A. Sassi, P. Tarwater, B. Ramratnam, P. Ruchala, R.I. Lehrer, A.J. Waring, and P. Gupta. (2010). The formulated microbicide RC-101 was safe and antivirally active following intravaginal application in pigtailed macaques. PLoS ONE. 5(11): e15111. (PMCID: PMC2993972)
    6. Micewicz E.D., A.L. Cole, C.L. Jung, H. Luong, M.L. Phillips, P. Pratikhya, S. Sharma, A.J. Waring, A.M. Cole, and P. Ruchala. (2010). Grifonin-1: a small HIV-1 entry inhibitor derived from the algal lectin, Griffithsin. PLoS ONE. 5(12): e14360. (PMCID: PMC3002932)
    7. Lamers, R.P., J.W. Stinnett, G. Muthukrishnan, C.L. Parkinson, and A.M. Cole. (2011). Evolutionary analyses of Staphylococcus aureus reveal that human nares harbor strains responsible for community- and hospital-acquired infections. PLoS ONE 6(1): e16426. (PMCID: PMC3025037)
    8. Martellini, J.A., A.L. Cole, P. Svoboda, O. Stuchlik, L.M. Chen, K.X. Chai, B.K. Gangrade, O.E. Sørensen, J. Pohl, and A.M. Cole. (2011). HIV-1 enhancing effect of prostatic acid phosphatase peptides is reduced in human seminal plasma. PLoS ONE. 6(1): e16285. (PMCID: PMC3024420)
    9. Sassi, A.B., M.R. Cost, A.L. Cole, A.M. Cole, D.L. Patton, P. Gupta and L.C. Rohan. (2011). Formulation development of Retrocyclin-1 (RC-101) as an anti-HIV vaginal microbicide product. Antimicrob Agents Chemother. 55(5): 2282-9. (PMCID: PMC3088226)
    10. Muthukrishnan, G., G.A. Quinn, R.P. Lamers, C. Diaz, A.L. Cole, S. Chen, and A.M. Cole. (2011). Exoproteome of Staphylococcus aureus reveals putative determinants of nasal carriage. J Proteome Res. 10(4): 2064-78. (PMCID:  PMC3070068)
    11. Sassi, A.B., K.E. Bunge, B.L. Hood, T.P. Conrads, A.M. Cole, P. Gupta, and L.C. Rohan. (2011). Preformulation and stability in biological fluids of the retrocyclin RC-101, a potential anti-HIV topical microbicide. AIDS Res Ther. 8(27): (Epub ahead of print). (PMCID: PMC3199744)
    12. Lamers, R.P., C.R. Eade, A.J. Waring, A.L. Cole, and A.M. Cole. (2011). Characterization of the retrocyclin analogue RC-101 as a preventative of Staphylococcus aureus nasal colonization. Antimicrob Agents Chemother. 55(11): 5338-46. (PMCID: PMC3195007)
    13. Ruchala, P., S. Cho, A.L. Cole, C. Carpenter, C.L. Jung, H. Luong, E.D. Micewicz, A.J. Waring, A.M. Cole, B.C. Herold, and R.I. Lehrer. (2011). Simplified theta-defensins: search for new antivirals. Int J Pept Res Ther. 17(4): 325-336.
    14. Li, M., D.L. Patton, Y. Cosgrove-Sweeney, D. Ratner, L.C. Rohan, A.M. Cole, P. Tarwater, P. Gupta, and B. Ramratnam. (2011). Incorporation of the HIV-1 microbicide cyanovirin-N in a food product. J AIDS. 58(4): 379-384. (PMCID: PMC3440868)
    15. Levinson, P., R.Y. Choi, A.L. Cole, T. Hirbod, S. Rhedin, B. Payne, B. Guthrie, R. Bosire, A.M. Cole, C. Farquhar, and K. Broliden. (2012). HIV-neutralizing activity of cationic polypeptides in cervicovaginal secretions of women in HIV-serodiscordant relationships. PLoS ONE. 7(2): e31996. (PMCID: PMC3289637)
    16. A.M.L. Edström, V. Rydengard, P. Fernlund, M. Morgelin, M. Baungarten, A.M. Cole, M. Malmsten, B.B. Karglund, O.E. Sørensen. (2012). beta-microseminoprotein endows seminal plasma with potent calcium-dependent candidacidal activity at vaginal pH. PLoS Pathogens. 8(4): e1002625. (PMCID: PMC3320615)
    17. Gupta, P., D. Ratner, M. Ding, B. Patterson, L.C. Rohan, T. Reinhart, V. Ayyavoo, X. Huang, D.L. Patton, B. Ramratnam, and A.M. Cole. (2012). Retrocyclin RC-101 blocks HIV-1 transmission across cervical mucosa in an organ culture. J AIDS. 60(5):455-461. (PMCID: PMC3404240)
    18. Gupta, P., C. Lackman-Smith, D. Ratner, L.C. Rohan, D.L. Patton, B. Ramratnam, and A.M. Cole. (2012). Antiviral activity of retrocyclin RC-101, a candidate microbicide against cell-associated HIV-1. AIDS Res Hum Retroviruses. 29(2): 391-6. (PMCID: PMC3552163)
    19. Lamers, R.P., G. Muthukrishnan, T. A. Castoe, S. Tafur, A.M. Cole*, and C.L. Parkinson*. (2012). Phylogenetic relationships among Staphylococcus species and refinement of cluster groups based on multilocus data. BMC Evol Biol. 12: 171. (PMCID: PMC3464590) *Equal correspondence/authorship.  Designated “Highly accessed” article by BMC.
    20. Eade, C.R., C. Diaz, M.P. Wood, K. Anastos, B.K. Patterson, P. Gupta, A.L. Cole, and A.M. Cole. (2012). Identification and Characterization of Bacterial Vaginosis-Associated Pathogens Using a Comprehensive Cervical-Vaginal Epithelial Coculture Assay. PLoS ONE. 7(11): e50106. (PMCID: PMC3499514)
    21. Eade, C.R., A.L. Cole, C. Diaz, L.C. Rohan, M.A. Parniak, P. Marx, P.M. Tarwater, P. Gupta, and A.M. Cole. (2013). The Anti-HIV Microbicide Candidate RC-101 Inhibits Pathogenic Vaginal Bacteria Without Harming Endogenous Flora or Mucosa. Am J Reprod Immunol. 69(2):150-8. (PMCID: PMC3541468)
    22. Wood, M.P., A.L. Cole, P. Ruchala, A.J. Waring, L.C. Rohan, P. Marx, P.M. Tarwater, P. Gupta, and A.M. Cole. (2013). A Compensatory Mutation Provides Resistance to Disparate HIV Fusion Inhibitor Peptides and Enhances Membrane Fusion. PLoS ONE. 8(2):e55478.  (PMCID: PMC3564752)
    23. Muthukrishnan, G., R.P. Lamers, A. Ellis, V. Paramanandam, A.B. Persaud, S. Tafur, C.L. Parkinson, and A.M. Cole. (2013). Longitudinal genetic analyses of Staphylococcus aureus nasal carriage dynamics in a diverse population. BMC Infect Dis. 16(13): 221. (PMCID: PMC3673815)
    24. Wood, M.P., A.L. Cole, C.R. Eade, L.M. Chen, K.X. Chai, and A.M. Cole. (2014). The HIV-1 gp41 ectodomain is cleaved by matriptase to produce a chemotactic peptide that acts through FPR2. Immunology. (in press)

    Recent Reviews/Book Chapters

    1. Sivaraman, K., N. Venkataraman, and A.M. Cole. (2009). Staphylococcus aureus nasal carriage and its contributing factors. Future Microbiol. 4: 999-1008. (PMCID: PMC2908500).
    2. Penberthy, W.T., S. Chari, A.L. Cole, and A.M. Cole. (2011). Retrocyclins and their activity against HIV-1. in:  Host-defense peptides: from biology to therapeutic strategies. Editor:  M. Luisa Mangoni. Cell Mol Life Sci. 68(13): 2231-42.
    3. Eade, C.R., M.P. Wood, A.M. Cole. (2012). Mechanisms and modifications of naturally occurring host defense peptides for anti-HIV microbicide development. Curr HIV Res. 10(1): 61-72.
    4. Lehrer, R.I., A.M. Cole, and M.E. Selsted. (2012). Theta Defensins: cyclic peptides with endless potential. J Biol Chem. 287(32):27014-9. (PMCID: PMC3411038)

    For more publication information, please visit Pubmed.

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    Dr. Amy Cole
  • Title: Research Associate Professor
  • Office: BMS 236
  • Phone: 407.823.0918
  • Send an Email
  • Biography:

    Our research interests include the study of several factors that modulate inflammatory pathways in the female genital tract (FGT). We have identified cationic antimicrobial peptides that contribute to the anti-viral capabilities of vaginal fluid. Former student projects have also identified pro-HIV molecules produced by endocervical cells exposed to bacterial vaginosis-associated bacteria. Current studies include fractionation of these co-culture fluids in order to identify specific proteins effecting epithelial barrier function, NFkB activation, and chemotaxis of HIV target cells. We collaborate with faculty from UCF and abroad in the pursuit of therapeutics that provide potent anti-viral activity without disturbing the dynamic environment of the FGT mucosa. We are also a GCLP-certified specimen processing lab for the HIV Vaccine Trials Network, and perform clinical processing for several Orlando-area clinical trials.

    Representative Publications:

    1. Venkataraman, N., Cole, A.L.*, Svoboda, P., Pohl, J, Cole, A.M. Cationic polypeptides are required for anti-HIV-1 activity of human vaginal fluid. J. Immunol. 175(11): 7560-7, 2005
    2. Cole, A.L., Yang, O.O., Warren, A.D., Waring, A.J., Lehrer, R.I., Cole, A.M. HIV-1 adapts to a retrocyclin with cationic amino acid substitutions that reduce fusion efficiency of gp41. J. Immunol. 176(11): 6900-5, 2006
    3. Cole, A.L., Herasimtschuk, A., Gupta, P., Waring, A.J., Lehrer, R.I., and Cole, A.M. The retrocyclin analogue RC-101 prevents human immunodeficiency virus type 1 infection of a model human cervicovaginal tissue construct. Immunology 121(1): 140-5, 2007
    4. Keller M.J., Guzman, E., Hazrati, E., Kasowitz, A., Cheshenko, N., Wallenstein, S., Cole, A.L., Cole, A.M., Profy, A.T., Wira, C.R., Hogarty, K., Herold, B.C. PRO 2000 elicits a decline in genital tract immune mediators without compromising intrinsic antimicrobial activity. AIDS. 21(4): 467-476, 2007
    5. Fuhrman, C.A., Warren, A.D., Waring, A.J., Dutz, S.M., Sharma, S., Lehrer, R.I., Cole, A.L., and Cole, A.M. Retrocyclin (RC)-101 overcomes cationic mutations on the heptad repeat 2 region of HIV-1 gp41. FEBS J. 274(24): 6477-87, 2007
    6. Cole, A.M., Cole, A.L. Antimicrobial polypeptides are key anti-HIV-1 effector molecules of cervicovaginal host defense. Am. J. Reprod. Immunol. 59(1): 27-34, 2008
    7. Martellini, J.A., Cole, A.L., Venkataraman, N., Quinn, G.A., Svoboda, P., Gangrade, B.K., Pohl, J., Sorensen, O.E., Cole, A.M. Cationic polypeptides contribute to the anti-HIV-1 activity of human seminal plasma. FASEB J. 23(10): 3609-18, 2009
    8. Cole, A.M., Patton, D.L., Rohan, L.C., Cole, A.L., Cosgrove-Sweeney, Y., Rogers, N.A., Ratner, D., Sassi, A., Tarwater, P., Ramratnam, B., Ruchala, P., Lehrer, R.I., Waring, A.J., and Gupta, P.  The formulated microbicide RC-101 was safe and antivirally active following intravaginal application in pigtailed macaques.  PLoS ONE 5(11): e15111, 2010.
    9. Sassi, A.B., Cost, M.R., Cole, A.L., Cole, A.M., Patton, D.L., Gupta, P., and Rohan, L.C.   Formulation development of Retrocyclin-1 (RC-101) as an anti-HIV vaginal microbicide product.  Antimicrob Agents and Chemother 55(5): 2282-9, 2011
    10. Martellini, J.A., Cole, A.L., Svoboda, P., Stuchlik, O., Chen, L.M., Chai, K.X., Gangrade, B.K., Sorensen, O.E., Pohl, J., and Cole, A.M.  HIV-1 enhancing effect of prostatic acid phosphatase peptides is reduced in human seminal plasma.  PLoS ONE 6(1): e16285, 2011.
    11. Ruchala, P., Cho, S., Cole, A.L., Carpenter, C., Jung, C-L., Luong, H., Micewicz, E.D., Waring, A.J., Cole, A.M., Herold, B.C., Lehrer, R.I. Simplified theta-defensins: search for new antivirals. Int. J. Peptide Res. and Ther. Published online Sept 23, 2011
    12. Levinson, P., Choi, R.Y., Cole, A.L., Hirbod, T., Rhedin, S., Payne, B., Guthrie, B.L., Bosire, R., Cole, A.M., Farquhar, C., Broliden, K. HIV-Neutralizing Activity of Cationic Polypeptides in Cervicovaginal Secretions of Women in HIV-Serodiscordant Relationships. PLoS One 2012; 7(2):e31996. Epub 2012 Feb 28
    13. Eade, C.R., Diaz, C., Wood, M.P., Anastos, K., Patterson, B.K., Gupta, P., Cole, A.L., Cole, A.M. Identification and characterization of bacterial vaginosis-associated pathogens using a comprehensive cervical-vaginal epithelial coculture assay. PLOS One. 7(11): 250106 Epub 2012 Nov15
    14. Eade, C.R., Cole, A.L.*, Diaz, C., Rohan, L.C., Parniak, M.A., Marx, P., Tarwater, P.M., Gupta, P., Cole, A.M. The anti-HIV microbicide candidate RC-101 inhibits pathogenic vaginal bacteria without harming endogenous flora or mucosa. Amer J Rep Immunol. 69(2): 150-8, 2013
    15. Wood, M.P., Cole, A.L., Ruchala, P., Waring, A.J., Rohan, L.C., Marx, P., Tarwater, P.M., Gupta, P., Cole, A.M. A compensatory mutation provides resistance to disparate HIV fusion inhibitor peptides and enhances membrane fusion. PLOS One. 8(2):e55478 Epub 2013 Feb5
    16. Wood. M.P., Cole, A.L., Eade, C.R., Chen, LM, Chai, K.X., Cole, A.M. The HIV-1 gp41 ectodomain is cleaved by matriptase to produce a chemotactic peptide that acts through FPR2. Accepted to Immunology, March 6, 2014
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