Shuxin Li, M.D., Ph.D.
Anatomy and Cell Biology, Shriners Hospitals Pediatric Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA
Shuxin Li Lab focuses on Axonal regeneration in the CNS, Neuronal repair, Spinal cord injury, and Cell death and neuronal survival. Following central nervous system (CNS) injury or with degenerative neurological disorders, loss of neuronal cells and axonal disconnection usually results in persistent dysfunction with a very limited recovery. So far, the medical treatments to enhance recovery from neurological deficits due to signal conduction failure are extremely restricted. Our longterm goals are to elucidate molecular and cellular mechanisms underlying neuronal damage and growth failure and to develop effective therapies to maximize recovery from neurological deficits caused by CNS axon damages, such as stroke, multiple sclerosis, and traumatic brain and spinal cord injuries. One area of our research is to characterize axonal growth inhibition mediated by extrinsic factors, such as myelinderived molecules and glial scarrelated proteoglycans. We have recently identified a functional receptor of LAR phosphatase that mediates axon growth inhibition by scarsourced inhibitors. We are also highly interested in exploring intracellular signaling pathways for regulating neuronal growth, including the reduced growth capacity of adult neurons in the CNS. Another emphasis of our studies is to understand the signaling mechanisms underlying neural cell death in the CNS after injuries. The final goal of our research is to develop successful therapeutic strategies for improving recovery from CNS injuries by promoting regeneration of axotomizedneurons and survival of injured neural cells. We have developed a number of small antagonist peptides which have great therapeutic potential for CNS lesions. To achieve our goal, we employ various in vitro and in vivo research approaches, including protein binding assays, genetic and pharmacological methods, neuronal cultures, neurite/axon growth analysis, in vivo axon lesion models, and behavioral evaluations in rodents..
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Stys PK, Li S. Glutamateinduced white matter injury: excitotoxicity without synapses. Neuroscientist. 2000; 6(4):230-33