Li Lab
Shuxin Li, MD, PhD
Assistant Professor of Neurology and Neuroscience Program
Office: ND4.124 Phone: 214-645-623 Fax: 214-645-6238
Lab: ND4.136
shuxin.li@utsouthwestern.edu
Following central nervous system (CNS) injury or with degenerative neurological disorders, loss of neuronal cells and axonal disconnection of surviving neurons usually result 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 long-term 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 myelin-derived molecules and glial scar-related proteoglycans. We are also highly interested in exploring the intracellular downstream 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 intracellular signaling mechanisms underlying neural cell death in the CNS after injuries. The final goal of our research is to develop more successful therapeutic strategies for improving recovery from CNS injuries by stimulating axon regeneration of axotomized-neurons and promoting survival of injured neural cells via targeting various molecules. To achieve our goal, we employ various in vitro and in vivo research approaches, including protein binding assays, genetic and pharmacological methods, neuronal cultures and neurite/axon growth analysis, in vivo axonal lesion models, and behavioral evaluations in rodents.
Selected Recent Publications
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 Strittmatter SM. Delayed systemic Nogo-66 receptor antagonist after spinal cord injury promotes recovery. J Neurosci, 2003; 23: 4219-4227. (Highlighted paper)
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. 2003. (*Co-first author)
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.
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, 2004; 24:10511- 10520. (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. 2005; 29: 26-39.
Cafferty W, Yang S, Duffy P, Li S and Strittmatter SM. Functional axonal regeneration through astrocytic scar genetically modified to digest chondroitin sulfate proteoglycans. J Neurosci, 2007, 27:2176-85.
Fu Q, Hue J and Li S. Nonsteroidal anti-inflammatory drugs promote axon regeneration via RhoA Inhibition. J Neurosci, 2007, 27:4154-64.
Dill J, Wang H, Zhou FQ and Li S. Inactivation of glycogen synthase kinase-3 promotes axonal growth and recovery in the CNS. J Neurosci, 2008, 28:8914-28. (Highlighted in Nat Med, 2008, 14 (10): 1027 and in Science-Business Exchange (SciBX), 2008, 1(36): 6-8).
Dill J, Patal AR, Yang X, Bachoo R, Powell CM and Li S. A Molecular Mechanism for Ibuprofen-mediated RhoA Inhibition in Neurons. J Neurosci, 2010, 30:963-72
Xing B, Li H, Wang H, Mukhopadhyay D, Fisher D, Gilpin CJ and Li S. RhoA-inhibiting NSAIDs promote axonal myelination after spinal cord injury. Exp Neurol, 2011, 231:247-260.
Fisher D, Xing B, Dill J, Li H, Hoang HH, Zhao Z, Yang XL, Bachoo R, Cannon S, Longo FM, Sheng M, Silver J and Li S. Leukocyte Common Antigen-Related Phosphatase Is a Functional Receptor for Chondroitin Sulfate Proteoglycan Axon Growth Inhibitors. J Neurosci, 2011, 31:14051-14066. (Highlighted paper).