Research

Pendurthi, Usha, Ph.D.

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Contact: usha.pendurthi@uthct.edu

Education:
Ph.D. in Biology - Osmania University, Hyderabad, India.
Post-doctoral Fellowship – Department of Medicine and Cancer Center, University of California, San Diego, CA.

Research Interest:
Hemostasis and Thrombosis; Role of blood clotting proteases in pathogenesis of cancer, inflammation and other diseases.

Research Overview:
Tissue factor (TF)-dependent blood coagulation plays primary role in hemostasis upon tissue injury but aberrant expression of TF leads to thrombotic disorders. The proper regulation of TF expression is critical not only for maintenance of the hemostatic balance but also health in general, and thus expression of TF activity on cell surfaces is tightly regulated. A part of our research focuses on understanding cellular mechanisms that regulate TF activity on cell surfaces.

Endothelial cell protein C receptor (EPCR) is a cellular receptor for protein C and activated protein C (APC). It is primarily localized on the endothelial cells of large blood vessels. Recent studies from our laboratory and others have shown that FVIIa, a clotting protease that binds to TF and initiates the activation of the coagulation cascade, also binds to endothelial cell protein C receptor (EPCR). FVIIa bound to EPCR on endothelial cells can activate PAR1-mediated cell signaling that provide barrier protective effect.

Both TF and EPCR, whose primary function is to regulate clotting, also affect various pathophysiological processes, including inflammation and cancer. Understanding of how TF-FVIIa- and EPCR-FVIIa-induced cell signaling pathways alters cellular functions and influence pathogenesis of cancer and inflammation is the primary focus of our research. Our recent studies show that introduction of EPCR expression to tumor cells through genetic engineering suppressed TF-driven tumor growth in malignant pleural mesothelioma. Studies are underway in identifying molecular mechanism by which EPCR suppresses tumor growth and evaluating therapeutic potential of EPCR-mediated pathway in curtailing tumor growth.

Selected Papers and Abstracts:

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