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My research focuses on the formation and destruction of a cellular structure called "myelin," which enwraps and insulates axons within the nervous system. A fatty substance, myelin allows for the fast conduction of the nerve's electrical signal and supports neuronal survival. Breakdown of the myelin, or demyelination, is a common pathologic feature in many neurodegenerative diseases, including multiple sclerosis, Charcot-Marie-Tooth syndrome, Guillian-Barre syndrome, and neuropathies secondary to diabetes and cancer chemotherapy. Because of the intimate connection between myelin and axons, the loss of myelin results in the loss of axonal integrity and neuronal functions with severe debilitating consequences. Therefore, preventing demyelination and promoting re-myelination are two important therapeutic objectives for the effective treatment of demyelinating neurodegenerative diseases.
The long-term objective of my research is to define molecular mechanisms that trigger myelin breakdown in the nervous system. I am also interested in elucidating mechanisms that promote re-myelination. I reason that aberrant signaling between myelinating glial cells and axons or the environment may underlie a wide range of demyelinating disorders. Understanding the signaling mechanisms that initiate myelin breakdown or promote re-myelination may have implication for the development of therapies to prevent further progression of the disease and to repair the demyelinated lesions.
My research team is currently investigating functions of growth factor signaling—especially those of erbB receptors—in regulating myelination and demyelination in the peripheral nervous system (PNS). We are also investigating functions of cadherins and the cytoplasmic effectors in promoting myelination. Studies to understand roles of Schwann cells, the myelin forming cells of the PNS, during injury and nerve repair are also being conducted.
21:120:355 Cell Biology
26:120:524 Cell, Molecular and Developmental Biology
26:120:526 Topics in Cell Biology: Signal Transduction
B.S. in Horticulture, Seoul National University, 1988.
M.S. in Biology, University of Toledo, 1990.
Ph.D. in Cell Biology, Neurobiology and Anatomy, University of Cincinnati, 1996.
Post-doc, Dana-Farber Cancer Institute, Harvard Medical School, 1997-2003.
Kim, H.A., Mindos, T., and D.B. Parkinson. Plastic Fantastic: Schwann cells and repair of the peripheral nervous system. Stem Cells Transl. Med. 2013
Yang, D.P., Kim, J., Syed, N., Tung, Y.J., Bhaskaran, A., Mindos, T., Mirsky, R., Jessen, K.R., Maurel, P., Parkinson, D.B., and H. A. Kim. p38 MAPK activation promotes denervated Schwann cell phenotype and functions as a negative regulator of Schwann cell differentiation and myelination. Journal of Neuroscience 2012 32 (21): 7158-7168.
Chen, Y., Wang, H., Yoon, S.O., Xu, X., Hottiger, M.O., Svaren, J., Nave, K.A., Kim, H.A., Olson, E.N., and Q.R. Lu. HDAC-mediated deacetylation of NF-κB is critical for Schwann cell myelination. Nature Neuroscience 2011 14 (4): 437-41.
Syed, N. and H. A. Kim. Soluble neuregulin and Schwann cell myelination: a therapeutic potential for improving remyelination of adult axons. Molecular and Cellular Pharmacology. 2010 2 (4): 161-167.
Syed, N., K. Reddy, D. P. Yang, C. Taveggia, J. L. Salzer, P. Maurel, and H. A. Kim. Soluble neuregulin-1 has bi-functional, concentration-dependent effects on Schwann cell myelination Journal of Neuroscience 2010 30: 6122-6131.
Kim, H. A. and P. Maurel. Primary Schwann cell cultures. 2009 Protocols for Neural Cell Cultures. 4th edition, Humana Press/Springer Media, 2009, in press.
Tyler, W.A., Gangoli, N., Gokina, P., H. A. Kim, M. Covey, S. Levison and T. L. Wood. Differentiation of oligodendrocytes requires activation of mammalian target of rapamycin signaling. Journal of Neuroscience. 2009 29 (19): p. 6367-6378.
Crawford, A., D. Desai, P. Gokina and H. A. Kim. E-cadherin expression in postnatal Schwann cell is induced by activation of cAMP-dependent protein kinase A pathway. Glia, 2008 56:1637-1647.
Yang, D. P., D. P. Zhang, K. S. Mak, D. E.Bonder, S. L. Pomeroy and H. A. Kim. Schwann cell proliferation during Wallerian degeneration is not necessary for regeneration and remyelination of the peripheral nerves: axon-dependent removal of newly generated Schwann cells by apoptosis. Molecular and Cellular Neuroscience, 2008 38(1): p. 80-88.
Ratner, N., J. Williams, J. J. Kordich and H. A. Kim. Schwann cell preparation from single mouse embryos: Analysis of neurofibromin function in Schwann cells. Methods in Enzymology. 2006 407: p 22-33.
Guertin, A., Zang, P. D., Mak, K. S., Alberta, J. A. and H. A. Kim. Microanatomy of axon/glial signaling resolved in artificial sciatic nerves. Journal of Neuroscience. 2005 25: p. 3478-3487.
Gray. P. A., H. Fu, P. Luo, Q. Zhao, J. Yu, A. Ferrari, T. Tenzen, D. Yuk, E. Tsung, Z. Cai, J. A. Alberta, L. Cheng, Y. Liu, J. M. Stenman, M. T. Valerius, N. Billings, H. A. Kim, A. P. McMahon, D. H. Rowitch, C. D. Stiles, and Q. Ma. Mouse Brain Organization Revealed through Direct Genome-scale TF expression analysis. Science 2004. 306 (5705): p. 2255-7.
Kim, H. A., N. Ratner, T. M. Roberts, and C. D. Stiles. Schwann cell proliferative responses to cAMP and Nf1 are mediated by cyclin D1. Journal of Neuroscience., 2001. 21(4): p. 1110-6.
Kim, H. A., S. L. Pomeroy, W. Whoriskey, I. Pawlitzky, L. I. Benowitz, P. Sicinski, C. D. Stiles, and T. M. Roberts. A developmentally regulated switch directs regenerative growth of Schwann cells through cyclin D1. Neuron., 2000. 26(2): p. 405-16.
Rosenbaum, T., H. A. Kim, Y. L. Boissy, B. Ling, and N. Ratner. Neurofibromin, the neurofibromatosis type 1 Ras-GAP, is required for appropriate P0 expression and myelination. Annals of the New York Academy of Sciences, 1999. 883: p. 203-14.
Kim H. A., and N. A. Ratner. Procedure for isolating Schwann cells developed for analysis of the mouse embryonic lethal mutation NF1. Cell Biology and Pathology of Myelin: Evolving Biological Concepts and Therapeutic Approaches eds. Devon RM, Doucette R, Juurlink BHJ, Nazarali AJ, Schreyer DJ, and Verge VMK. Plenum press, New York, 1997, p 201-212.
Rosenbaum, C., S. Karyala, M. A. Marchionni, H. A. Kim, A. L. Krasnoselsky, B. Happel, I. Isaacs, R. Brackenbury, and N. Ratner. Schwann cells express NDF and SMDF/n-ARIA mRNAs, secrete neuregulin, and show constitutive activation of erbB3 receptors: evidence for a neuregulin autocrine loop. Experimental Neurology., 1997. 148(2): p. 604-15.
Kim, H. A., B. Ling, and N. Ratner. Nf1-deficient mouse Schwann cells are angiogenic and invasive and can be induced to hyperproliferate: reversion of some phenotypes by an inhibitor of farnesyl protein transferase. Molecular & Cellular Biology., 1997. 17(2): p. 862-72.
Kim, H. A., J. E. DeClue, and N. Ratner. cAMP-dependent protein kinase A is required for Schwann cell growth: interactions between the cAMP and neuregulin/tyrosine kinase pathways. Journal of Neuroscience Research., 1997. 49(2): p. 236-47.
Wrabetz, L., M. L. Feltri, H. Kim, M. Daston, J. Kamholz, S. S. Scherer, and N. Ratner. Regulation of neurofibromin expression in rat sciatic nerve and cultured Schwann cells. Glia., 1995. 15(1): p. 22-32.
Kim, H. A., T. Rosenbaum, M. A. Marchionni, N. Ratner, and J. E. DeClue. Schwann cells from neurofibromin deficient mice exhibit activation of p21ras, inhibition of cell proliferation and morphological changes. Oncogene., 1995. 11(2): p. 325-35.