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Department of Pharmacology & Toxicology
Department of Microbiology and Immunology
Medical College of Wisconsin
PhD, Marquette University, 1989
Platelets are important in early wound healing, where they initially adhere to the extracellular matrix that underlies damaged blood vessels and then aggregate with one another to form a platelet plug. Excessive bleeding occurs when platelet counts are low, or when platelet activity is compromised. Children, especially neonates, who underdo cardiac surgery for repair of congenital heart defects experience excessive bleeding at higher rates than do adults undergoing similar surgeries. We seek to determine the extent to which deficiencies in platelet number or function contribute to excessive bleeding in the setting of pediatric cardiac surgery. This research will help physicians identify pediatric cardiac surgery patients who are at risk for bleeding and administer appropriate blood products in a timely manner should bleeding need to be controlled in this setting.
A major focus of research in our laboratory is Platelet Endothelial Cell Adhesion Molecule-1 (PECAM-1). PECAM-1 is an inhibitory molecule that functions in two important contexts. First, PECAM-1 dampens platelet aggregation in response to low levels of stimulation, which is important to prevent pathological thrombosis. Second, PECAM-1 inhibits T cell responses and interferes with the ability of T cells to kill tumors. We have recently discovered that the ability of PECAM-1 to inhibit T cell anti-tumor responses depends on Transforming Growth Factor β (TGFβ), which is another potent T cell suppressor. Our current work is dedicated to development of a better understanding of how PECAM-1 and TGFβ work together to inhibit T cell responses. This research will help us improve T cell-based therapies for treatment of cancer.
NIH, R35-HL139937 (Co-Investigator), ‘Basic Investigation & Translational Applications Concerning the Cell & Molecular Biology of Blood & Vascular Cells (2018-2024)
Research Associate II