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Hometown: Elmont, NY Undergraduate University: Stony Brook University Undergraduate Major: Biochemistry Graduate Advisor: Dr. Stella Tsirka Graduate Program: Molecular and Cellular Pharmacology email: emmets at pharm.stonybrook.edu

Research Interests: The Role of Microglia, Tissue Plasminogen Activator and Zinc in Spinal Cord Injury

I investigate the link between microglia, tissue plasminogen activator (tPA) and zinc in spinal cord regeneration. Injury to the spinal cord induces an immune response in which microglia, the resident immuno-competent cells of the central nervous system, migrate to the site of injury and become activated. Microglial activation is thought to contribute to secondary damage following the initial injury. However, controversy still exists over the neurodegenerative versus neuroregenerative roles of activated microglia. Once activated, microglia secrete neurotrophic and neurotoxic factors, as well as tPA. Under normal physiological conditions, the proteolytic activity of tPA functions in extracellular matrix remodeling and neurite outgrowth. During pathological events tPA levels increase, which enhances microglial activation. Activation of microglia, apoptotic cell death and neural damage has been shown to be significantly reduced in tPA-/- mice after injury. Another factor that may affect the activation of glial cells, gliosis, is zinc. Zinc is concentrated in the dorsal and ventral horns of the spinal cord and is thought to have a major impact on neuronal damage. In spinal cord injury (SCI), gliosis occurs prior to the formation of the inhibitory glial scar, which acts as a barrier to neurite outgrowth. We have previously demonstrated that tPA has a neuroprotective effect against zinc toxicity and may act as a zinc chelator. Binding of zinc to tPA also decreases tPA proteolytic activity. It is unknown whether extracellular chelatable zinc plays a role in the outcome after SCI. I currently explore the possibility that zinc regulates microglial activation by binding tPA, which could lead to a decrease in secondary injury following the initial insult to the spinal cord.