Medical Student Research Fellowship for Summer 2005

Mentor: Shuxin Li
Department: Neurology
Room number: F2.212A
Mail Code: 9036
Phone number: 89370
E-mail: shuxin.li@utsouthwestern.edu
Project title: Promoting neuronal regeneration and repair in the damaged central nervous system

Human subjects IRB approved project number (where applicable):

Animal subjects IRB approved project number (where applicable): 1040-04-01-1

Project Type (patient-based research, animal-based research, or basic research; this characterization is only to permit a general classification for grouping similar types of projects): both animal-based and basic research

Brief Description of Project:

Following injury in the central nervous system (CNS) injury, or with the degenerative neurological disorders, axonal disconnection of surviving neurons or loss of neuronal cells may result in persistent dysfunction with a very limited recovery. Promotion of axonal regrowth and neuronal survival are essential for injury repair in the CNS. My research is focused on the cellular and molecular mechanisms underlying the failure of axonal regeneration and cell death in the damaged CNS. One area of our research is to characterize axonal growth inhibition mediated by extrinsic factors, such as myelin-derived molecules and glial scar-related proteoglycans, and regulated by the intracellular downstream signaling pathways. Another emphasis of our studies is to understand the intracellular signaling mechanisms underlying the neural cell death in the CNS after injury. The final goal of our research is to develop potential therapeutic strategies for improving recovery from CNS injury by stimulating axonal regeneration in surviving axotomized-neurons and by promoting the survival of injured neural cells via targeting various molecules.

Previous Research Activities or Publications with Medical Students:

" Li S, Liu BP, Budel S, Li M, Ji B, Walus L, Jirik A, Rabacchi S, Choi E, Worley D, Sah DWY, Pepinsky B, Lee D, Relton J and Strittmatter SM. Blockade of Nogo-66, MAG plus OMgp by soluble Nogo-66 receptor promotes axonal sprouting and recovery after spinal injury. J Neurosci, 24: 10511-10520, 2004. (Highlighted paper).
" Li S, Kim JK, Budel S, Hampton TG and Strittmatter SM. Transgenic inhibition of Nogo-66 receptor function allows axonal sprouting and improved locomotion after spinal injury. Mol Cell Neurosci, 2004, in press.
" Kim JK*, Li S*, GrandPre T, Qiu K, Greer CA and Strittmatter SM. Axon Regeneration in young adult mice lacking Nogo-A/B. Neuron, 2003; 38: 187-199. 2003. (*Co-first author).
" Li S and Strittmatter SM. Delayed systemic Nogo-66 receptor antagonist after spinal cord injury promotes recovery. J Neurosci, 2003; 23: 4219-4227. (Highlighted paper).
" Zheng B, .Ho C, .Li S, Keirstead H, Steward O, Tessier-Lavigne M. Lack of enhanced spinal regeneration in Nogo deficient mice. Neuron 2003; 38: 213-224.
" GrandPré T*, Li S * and Strittmatter SM. Nogo-66 receptor antagonist peptide promotes axonal regeneration. Nature, 2002; 417: 547-551. (*Co-first author).
" Li S and Stys PK. Mechanisms of ionotropic glutamate receptor-mediated excitotoxicity in isolated spinal cord white matter. J Neurosci 2000; 20: 1190-1198. (Cover Figure)
" Li S, Mealing GAR, Morley P, Stys PK. Novel injury mechanism in anoxia and trauma of spinal cord white matter: glutamate release via reverse Na+-dependent glutamate transport. J Neurosci 1999; 19: RC 16(1-9). (Cover Figure)

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