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Axon regrowth study on rodent spinal cord injury model Do-Hun Lee, Ph.D. Department of Medical and Molecular Genetics, Stark Neurosciences Research Institute Indiana University School of Medicine Spinal cord injury patients have permanent paralysis that results from the failure of regeneration of damaged axon after injury. The major reason for this lack of regeneration is the presence of intrinsic inhibitory molecules in nerve cells and the extrinsic inhibitory environment of the Central Nervous System. Spinal cord injury studies require diverse techniques such as animal surgery, tissue engineering, and 3D- imaging. Dr. Lee’s research has focused on studying mechanisms of both intrinsic and extrinsic inhibitors of axon regeneration to determine combinatorial approaches to promote functional recovery after spinal cord injury. Dr. Lee will talk about how intrinsic and extrinsic inhibitors block the axon re-growth and functional recovery after spinal cord injury. Phosphatase and tensin homolog (PTEN) is an intrinsic inhibitor of retinal ganglion cell axon regeneration. PTEN deletion or Chondroitin sulfate proteoglycans (CSPGs) degradation by chondroitinase ABC (chABC) has been shown to induce axonal re-growth in previous studies. However, the regeneration was limited. He decided to try a combinatorial approach to target both intrinsic (PTEN) and extrinsic (CSPGs) inhibitors to promote axon regeneration after injury. His works have an additive effect of the combined treatment. PTEN deletion and chABC treatment are sufficient to increase corticospinal tract axon sprouting using a pyramidotomy injury model, indicating enhanced axonal growth after injury. He will also talk about developing techniques using 3D projections to trace regenerating axons in vivo after spinal cord injury using a light sheet fluorescence microscopy. His works using this pioneer technique have shown Confocal image of gastrocnemius motor neurons labeled with CTB-Alexa 555 and sensory fiber terminals labeled with AAV8-UbC-GFP in the cleared rat lumbar spinal cord.
Transcript of €¦ · Web viewafter spinal cord injury using a light sheet fluorescence microscopy. His works...
Axon regrowth study on rodent spinal cord injury model
Do-Hun Lee, Ph.D.Department of Medical and Molecular Genetics, Stark Neurosciences Research Institute
Indiana University School of Medicine
Spinal cord injury patients have permanent paralysis that results from the failure of regeneration of damaged axon after injury. The major reason for this lack of regeneration is the presence of intrinsic inhibitory molecules in nerve cells and the extrinsic inhibitory environment of the Central Nervous System. Spinal cord injury studies require diverse techniques such as animal surgery, tissue engineering, and 3D-imaging. Dr. Lee’s research has focused on studying mechanisms of both intrinsic and extrinsic inhibitors of axon regeneration to determine combinatorial approaches to promote functional recovery after spinal cord injury. Dr. Lee will talk about how intrinsic and extrinsic inhibitors block the axon re-growth and functional recovery after spinal cord injury.
Phosphatase and tensin homolog (PTEN) is an intrinsic inhibitor of retinal ganglion cell axon regeneration. PTEN deletion or Chondroitin sulfate proteoglycans (CSPGs) degradation by chondroitinase ABC (chABC) has been shown to induce axonal re-growth in previous studies. However, the regeneration was limited. He decided to try a combinatorial approach to target both intrinsic (PTEN) and extrinsic (CSPGs) inhibitors to promote axon regeneration after injury. His works have an additive effect of the combined treatment. PTEN deletion and chABC treatment are sufficient to increase corticospinal tract axon sprouting using a pyramidotomy injury model, indicating enhanced axonal growth after injury. He will also talk about developing techniques using 3D projections to trace regenerating axons in vivo after spinal cord injury using a light sheet fluorescence microscopy. His works using this pioneer technique have shown successful regeneration of injured specific axon tracts after spinal cord injury. He has utilized this 3D imaging technique to identify candidate genes involved in axon regeneration after spinal cord injury.
Biography: Dr. Lee is a Research Associate of the Department of Medical and Molecular Genetics, Stark Neurosciences Research Institute, Indiana University School of Medicine. Dr. Lee received his doctorate degree in Neuroscience from Seoul National University of South Korea. His graduate works covered a wide range of neuroscience, including stem cell therapy for brain tumor formation, traumatic brain injury, neurogenesis, spinal cord injury. During his postdoctoral fellow in University of Miami Miller School of Medicine, his studies had focused on understanding of what happens in damaged neurons after spinal cord injury. He also had focused on how we could protect spinal cord from further damage after injury and promote axon re-growth to allow maximum potential for functional recovery. His challenge was not limited in axon regeneration studies. He has also tried to find possible therapeutic targets again Alzheimer’s disease using rodent animal model in Mayo Clinic in Jacksonville Florida.Currently, his research interest has focused on understanding mechanisms of anti-sense oligonucleotides therapeutic methods in Alzheimer’s disease in Indian University.
Confocal image of gastrocnemiusmotor neurons labeled with CTB-Alexa 555 and sensory fiber terminals labeled with AAV8-UbC-GFP in the cleared rat lumbar spinal cord.
