Dr. Rao joined The University of Texas Health Science at Tyler in 1993. He is currently tenured professor in the Department of Cellular and Molecular Biology and holds The Dr. and Mrs. James Vaughn Professorship in Biomedical Research. He received his post-doctoral training in the Department of Medicine at the University of California San Diego and joined in the faculty rank upon completion of his training at the same university before he moved to UTHSCT. He served in many leadership roles at the institution including as the Faculty Senate Chair. His research is continuously supported by grant funding from NIH, American Heart Association and pharmaceutical industry. He acted as a reviewer for many national and international granting agencies including NIH, AHA, Department of Veteran Affairs, The Wellcome Trust Fund, The Israel Science Foundation, The Netherlands Organization for Health Research and Development, Belgium Research Council, and Royal Swedish Academy. He also served as Associate Editor to Arteriosclerosis, Thrombosis, and Vascular Biology and Editorial Member for Haemostasis and Journal of Thrombosis and Haemostasis, and reviews manuscripts for more than 50 scientific journals. Dr. Rao published more than 160 peer-reviewed articles and trained more than 30 PhD or MD post-doctoral fellows and several PhD students registered at other universities.

Dr. Rao’s lab is researching in understanding the regulation of prothrombotic cofactors that contribute to thrombosis in a variety of disease and how hemophilia therapy could be improved and make it cost effective. Abnormalities in the blood clotting process lead to either thrombosis (excessive blood clotting) or bleeding disorders (lack of blood clotting; e.g., hemophilia). Thrombosis is the primary cause of heart attacks and strokes. They account more deaths worldwide than any other diseases including all cancers and infectious diseases combined. Hemophilia is a bleeding disorder and bleed profusely following surgery or injury. The bleeding in hemophilia could be life-threatening if not treated promptly. Chronic minor bleeding into joints in hemophilia may lead to joint disease with debilitating pain, which could be prevented or reduced by prophylactic treatment.

Education & Training

University of California San Diego
Post-Doctoral Fellowship
Jawaharlal Nehru University
PhD, Life Sciences
Jawaharlal Nehru University
MPhil, Life Sciences
Osmania University
MS, Genetics

Courses Taught

BIOT 5222 - Advanced Metabolism
BIOT 5222L - Advanced Metabolism Lab
BIOT 5310 – Fundamental of Biomedical Research

Research Interest

Cellular dynamics that regulate procoagulant cofactor (tissue factor, TF) activity at cell surfaces and molecular mechanisms responsible for TF encryption and decryption Establishing the pathophysiological significance of factor VIIa interaction with endothelial cell protein C receptor (EPCR) Mechanisms by which TF and EPCR contribute or influence pathogenesis of various diseases, including thrombosis, hemophilia, cancer, and inflammation

Publication Highlights

Kondreddy V, Wang J, Keshava S, Esmon CT, Rao LVM, Pendurthi UR. Factor VIIa induces anti-inflammatory signaling via EPCR and PAR1. Blood 131:2379-2392, 2018. Wang J, Pendurthi UR, Rao LVM. Sphingomyelin encrypts tissue factor: ATP-induced activation of A-SMase leads to tissue factor decryption and microvesicle shedding. Blood Advances, DOI 10.1182/blood advances.2016003947, 2017.
Keshava S, Sahoo S, Tucker TT, Idell S, Rao LVM, Pendurthi UR. Opposing effects of tissue factor and endothelial cell protein C receptor on tumor growth of malignant pleural mesothelioma. Cancer Research 73: 3963-3973, 2013.
Sen P. Gopalakrishnan R, Kothari H, Clark C, Keshava S, Esmon CT, Pendurthi UR, Rao LVM. Factor VIIa bound to endothelial cell protein C receptor activates protease activated receptor-1 and mediates cell signaling and barrier protection. Blood 117, 3199-3208, 2011.
Hjortoe GM, Petersen LC, Albrektsen T, Sorensen BB, Norby PL, Mandal S, Pendurthi UR, Rao LVM. Tissue factor-factor VIIa specific up-regulation of IL-8 expression in MDA-MB-231 cells is mediated by PAR-2 and results in increase cell migration. Blood 103, 3029-3037, 2004.