Qun Li, M.D., Ph.D.

Kennedy Krieger Institute
707 N. Broadway
Baltimore, MD 21205
Phone: (443) 923-9239
Email: liq@kennedykrieger.org

Dr. Qun Li is a research scientist at the International Center for Spinal Cord Injury, Hugo W. Moser Institute, at Kennedy Krieger.

Biographical Sketch:

Dr. Qun Li graduated and earned a medical degree from Beijing Medical University. He received his doctoral degree in neurobiology from the Ohio State University (Drs. Beattie/Bresnahan's lab) in 1996. After five years post-doctoral training at the NIH (NICHD), St. Louis University and Columbia University in neuroscience, he started working with Dr. John McDonald in the Department of Neurology at Washington University in St. Louis as a research instructor in 2001. Dr. Qun Li joined the International Center for Spinal Cord Injury at the Kennedy Krieger Institute in 2005.

Research Summary:

Dr. Qun Li’s long-term research goal is to investigate the plasticity and regeneration of traumatically injured spinal cord and to develop novel repair strategies to improve anatomical reorganization and functional recovery in experimental model of spinal cord injury (SCI). Currently, he is mainly focusing on the following areas of interest:

1. Embryonic stem (ES) cell transplantation in SCI: Mouse ES cells are induced to neural progenitors with 4-/4+ protocol (four days without, then four days with retinoic acid in culture). After transplanted into contusive injured rat spinal cord, ES cells survive, migrate and produce permissive extracellular matrix (ECM), such as laminin and fibronectin, which promote damaged axons regenerating and passing through the lesion site. ES cell grafts also produce matrix metalloproteinases (MMPs) and degrades inhibitory molecule chondroitin sulfate proteoglycan (CSPG) and astrocyte scar. As a result, ES cell transplantation promotes axonal regeneration of long descending pathway (such as corticospinal tract CST) in SCI. Transplanted high-purity of oligodendrocytes derived from ES cells remyelinat the spared axons in injured spinal cord. The remyelination not only promotes the recovery of locomotion behavior but also limits sprouting of nociceptive afferent fibers and attenuates neuropathic pain in SCI.
2. Activity dependent development of endogenous neural stem cells (eNSCs) in the spinal cord: The proliferating eNSCs in spinal cord are detected by BrdU labeling. The phenotypes of these newborn cells are confirmed as glial progenitors including oligodendrocyte progenitor cells (OPCs) or mature oligodendrocytes with double-immunostaining of BrdU with selective markers (Nestin, NG2, APC, etc.). The electrical activity in the spinal cord determines the development of these myelinating glial cells. Administration of reagents blocking neural activity (such as GABA-B receptor agonist Baclofen) decreases, but electrical stimulation on axons of corticospinal tract increases proliferation and differentiation of OPCs. These studies have important implications for harnessing activity to promote myelination after demyelination and may offer new approaches to the treatment of diseases including multiple sclerosis (MS) and spinal cord injury (SCI).