UVA Neuroscience Graduate Program

Astrocytes are the most numerous cell type in the brain and perform multiple functions in development and maturity. These cells, also known as astroglia, respond to diverse forms of neural injury with a complex but poorly understood phenotypic change, termed reactive astrogliosis. Like the immune response, astrogliosis has both beneficial and detrimental consequences. The response is classically defined by cell hypertrophy and process extension, glial filament upregulation, and in some cases, proliferation and migration. MAP kinase (MAPK) signaling pathways were classically characterized as effectors of mitogenic and stress stimuli, but are recently implicated in the regulation of cell motility. Our preliminary in vitro data indicate that astroglial process extension and migration are differentially modulated by the ERKMAPK and the p38MAPK pathways. The broad objective of the proposed research program is to define specific roles for and mechanisms by which these two MAPK modules modulate the morphology and motility of reactive astroglia. Experiments employ established in vitro and in vivo techniques as well as Cre/lox conditional gene inactivation approaches. It is anticipated that knowledge gained from these studies will lead to a greater understanding of astroglial involvement in neurological diseases, and lead to development of targeted therapies to therapeutically modulate astrogliosis.

• NIH Style Biographical Sketch