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rarmstrong@usuhs.mil
Ph.D. University of North Carolina at Chapel Hill
NEURAL PROGENITOR CELLS IN CNS DEVELOPMENT AND REPAIR
Developmental abnormalities and pathological processes can cause severe neurological dysfunction. Our lab's current research activities focus on the cellular and molecular mechanisms that regulate neural cell development and regeneration. Approaches used in the lab include cell culture, histology, immunofluorescence, in situ hybridization, transgenic and knockout mouse lines, retroviral lineage tracing, gene cloning and transfection, RNA interference, and gene arrays. We use these tools to study the growth factors and transcription factors that regulate the proliferation, migration, differentiation, and survival of neural progenitor cells. Current experiments examine the role of fibroblast growth factor as an inhibitor of differentiation of precursors of oligodendrocytes into mature oligodendrocytes, and the role of platelet-derived growth factor in stimulating proliferation and enhancing survival of the progenitor cells. In vivo progenitor cell proliferation, migration, differentiation, and survival are being studied during development and in adult rodent CNS after experimental myelin damage, or demyelination. Demyelination causes neurological dysfunction in several human diseases, the most common being multiple sclerosis. In multiple sclerosis myelin repair, or remyelination, is insufficient and recovery of function is incomplete. In one virally induced experimental model studied, demyelinated areas, with oligodendrocyte and myelin loss, are efficiently remyelinated. We are identifying the roles of specific growth factors from lesioned areas that trigger progenitor cells around a lesion to generate replacement cells for remyelination and recovery of neurologic function. In a second neurotoxicant model of demyelination, either acute or chronic disease states can be studied to determine differences in repair responses of progenitor cells in each lesion environment. By comparing analysis of development and multiple disease models, we can determine the regulatory signals that are dominant in each tissue environment. This information will be important for extending the findings to the diverse diseases in humans that have loss of function primarily due to demyelination or that is more extensive due to demyelination, including multiple sclerosis, leukodystrophies, spinal cord injury, traumatic brain injury, and ischemic or toxic insults.
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