Zhigang He
Zhigang He, Ph.D., B.M. Professor of Neurology Boston Children's Hospital F.M. Kirby Neurobiology Center Center for Life Science Boston, MA 02115, USA About Zhigang He Zhigang He received his PhD from the University of Toronto and was a postdoctoral fellow with Marc Tessier-Lavigne at the University of California, San Francisco. He has the honor of being named a Klingenstein Fellow in Neuroscience, a John Merck Scholar and a McKnight Scholar. Dr. He is the director of the Boston Children’s Hospital Viral Core, which aims to provide technological resources to academic investigators interested in the development and use of viral based vectors. The Boston Children’s Hospital Viral Core aims to provide technological resources to academic investigators interested in the development and use of viral based vectors. Currently, we offer custom lentiviral vector production, custom AAV vector production with a variety of serotypes and aliquots of in-stock vector. The Viral Core is located on the 13th floor of the Center for Life Science building. Research Overview Zhigang He is interested in why lesioned axons cannot regenerate in the adult mammalian central nervous system (CNS). His research has been focused on two potential mechanisms: the inhibitory activity in the adult lesion sites and reduced intrinsic ability associated with mature CNS neurons. Previous studies indicate that the inhibitory activity is principally associated with components of CNS myelin and molecules in the glial scar at the lesion site. Recent studies from He's laboratory and others suggested that three myelin proteins -- myelin-associated glycoprotein (MAG), Nogo-A and oligodendrocyte myelin glycoprotein (OMgp) -- collectively account for the majority of the inhibitory activity in CNS myelin. The inhibitory activity of MAG, OMgp and the extracellular domain of Nogo-A might be mediated by a receptor complex with a Nogo receptor and at least two co-receptors, p75/TROY and Lingo-1. Blocking such inhibitory activity by genetic and pharmacological approaches could promote local axonal sprouting and reactivate structural plasticity but is not sufficient to allow long-distance axon regeneration. Our current studies are aimed to define cellular and molecular mechanisms underlying the intrinsic regenerative capacity of mature neurons. He and his colleagues envision two main possibilities for the lack of axon re-growth responses after an injury: (1) the signals carrying information of axotomy fail to reach to the cell body for activating regenerative program; and/or (2) the axonal growth program could not to be reactivated even if the retrograde signals are delivered to the cell bodies. They are addressing these issues by a combination of in vitro and in vivo approaches.
Selected Recent Publications Lu Y, Belin S, He Z (2014) Signaling regulations of neuronal regenerative ability. Curr Opin Neurobiol 27C:135-142. O'Donovan KJ, Ma K, Guo H, Wang C, Sun F, Han SB, Kim H, Wong JK, Charron J, Zou H, Son YJ, He Z, Zhong J (2014) B-RAF kinase drives developmental axon growth and promotes axonregeneration in the injured mature CNS. J Exp Med 211:801-814. Ho PP, Kanter JL, Johnson AM, Srinagesh HK, Chang EJ, Purdy TM, van Haren K, Wikoff WR, Kind T, Khademi M, Matloff LY, Narayana S, Hur EM, Lindstrom TM, He Z, Fiehn O, OlssonT, Han X, Han MH, Steinman L, Robinson WH (2012) Identification of naturallyoccurring fatty acids of the myelin sheath that resolve neuroinflammation. Sci Transl Med 4:137ra73. Jiang L, Qin X, Zhong X, Liu L, Jiang L, Lu Y, Fan L, He Z, Chen Q (2011) Glycine-inducedcytoprotection is mediated by ERK1/2 and AKT in renal cells with ATP depletion. Eur J Cell Biol 90:333-341. Park KK, Liu K, Hu Y, Kanter JL, He Z (2010) PTEN/mTOR and axon regeneration. Exp Neurol 223:45-50.
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