Faculty and Research

Biography

 

Courses in which I teach include Quantitative Biological Methods BSC3403C, Biomedical Chemistry BCH4024, Experimental Molecular Cell Biology PCB4529C and Molecular Biology PCB3522. I am also a co-coordinator of the BSBS Clinical Internship Program.

My interest in mentoring undergraduate students in research (such as through PILOT PCB4943) stems from my previous research in the field of neuroregeneration.  Spinal cord injury affects about 280,000 people in the U.S.  After injury to the central nervous system, neurons are faced with a complex milieu in the lesion environment, resulting in failure of regrowth across the injury site. One inhibitory factor that is secreted by hypertrophic astrocytes is chondroitin sulfate proteoglycan (CSPG). By using an in vitro model of the glial scar that incorporates CSPGs, we can determine factors that may be beneficial for enhancing regeneration in vivo.  I am also interested in investigating the intracellular machinery that may need to be upregulated during regeneration through gene therapy in order to promote robust growth post-injury.

 

Recent Publications:

Research Articles

  1. J.S. Simske, M. Koppen, P. Sims, J. Hodgkin, A. Yonkof and J. Hardin. The cell junction protein VAB-9 regulates adhesion and epidermal morphology in C. elegans. Nature Cell Biology 5(7):619-625 (2003). http://www.ncbi.nlm.nih.gov/pubmed/12819787
  2. J.M. Massey, J. Amps, M.S. Viapiano, R.T. Matthews, M.R. Wagoner, C.M. Whitaker, W. Alilain, A.L. Yonkof, A. Khalyfa, N.G.F. Cooper, J. Silver and S.M. Onifer. Increased chondroitin sulfate proteoglycan expression in denervated brainstem targets following spinal cord injury creates a barrier to axonal regeneration overcome by chondroitinase ABC and neurotrophin-3. Experimental Neurology 209(2):426-445 (2008). http://www.ncbi.nlm.nih.gov/pubmed/17540369
  3. K.P. Horn, S.A. Busch, A.L. Hawthorne, N. van Rooijen and J. Silver. Another barrier to regeneration in the CNS: Activated macrophages induce extensive retraction of dystrophic axons through direct physical interactions. J Neurosci. 28(38):9330-9341 (2008). http://www.ncbi.nlm.nih.gov/pubmed/18799667
  4. S.A. Busch, K.P. Horn, F.X. Cuascut, A.L. Hawthorne, L. Bai, R. Miller, and J. Silver. Adult NG2+ cells are permissive to neurite outgrowth and stabilize sensory axons during macrophage-induced axonal dieback after spinal cord injury. J Neurosci. 30(1):255-65 (2010). http://www.ncbi.nlm.nih.gov/pubmed/20053907
  5. A.L. Hawthorne, C.J. Wylie, L.T. Landmesser, E.S. Deneris and J. Silver. Serotonergic neurons migrate radially through the neuroepithelium by dynamin-mediated somal translocation. J Neurosci. 30(2):420-30 (2010). http://www.ncbi.nlm.nih.gov/pubmed/20071506
  6. A.L. Hawthorne, H. Hu, B. Kundu, M.P. Steinmetz, C.J. Wylie, E.S. Deneris, and J. Silver. The unusual response of serotonergic neurons after CNS injury: lack of axonal dieback and enhanced sprouting within the inhibitory environment of the glial scar. J Neurosci. 31(15): 5605-16 (2011). http://www.ncbi.nlm.nih.gov/pubmed/21490201

Reviews

  1. A.L. Hawthorne and P.G. Popovich. Emerging concepts in myeloid cell biology after spinal cord injury.  Neurotherapeutics 8(2): 252-61 (2011). http://www.ncbi.nlm.nih.gov/pubmed/21400005
  2. A.L. Hawthorne. Repurposing Reelin: the new role of radial glia, Reelin and Notch in motor neuron migration. Experimental Neurology 256:17-20 (2014). doi: 10.1016/j.expneurol.2014.02.024. Epub 2014 Mar 5. http://www.ncbi.nlm.nih.gov/pubmed/24607503

Book Chapter

  1. J. Silver, K.P. Horn, S.A. Busch and A.L. Yonkof. Neural regeneration: regeneration and functional recovery: Axonal regeneration: role of the extracellular matrix and the glial scar. The New Encyclopedia of Neuroscience 2009. Eds. Larry Squire, Tom Albright, Floyd Bloom, Fred Gage, and Nick Spitzer. Oxford: Elsevier, 1173-1180 (2007).

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