Postdoctoral Research Associate
University of North Carolina at Chapel Hill
Chapel Hill, North Carolina, United States
I am Nirupama Ramadas, PhD, Postdoctoral Research Associate at Dr. Erica Sparkenbaugh's lab, Blood Research Center, University of North Carolina at Chapel Hill.
I completed my Ph.D from Mysore University, India. During my doctoral work I investigated the role of chronic stress on glucose metabolism. I had my initial postdoctoral training in SASTRA University, India. I was awarded with Young Scientist Fellowship from Indian Council of Medical Research for the project entitled “Impact of Gestational Diabetes Mellitus on feto-placental vascular function”. I joined as postdoctoral fellow in Dr. He’s lab, in the Department of Cellular and Molecular Physiology, Penn State College of Medicine, Hershey, where my work was focused on delineating the mechanisms involved in long-term exercise-induced attenuation of atherosclerotic progression in Apo E KO mice. I joined Dr. Erica Sparkenbaugh's lab at University of North Carolina in December 2021. My research project is focuses on the investigation of biased protease activated receptor 1 (PAR1) signaling to attenuate the vascular complications associated with VOC (Vaso Occlusive Crisis) including enhanced thromboinflammation and microvascular stasis in sickle cell disease (SCD). SCD is a most common inherited hemoglobinopathy caused by a single nucleotide mutation in the β- globin chain. Chronic activation of coagulation and inflammation mediates disease pathology. PAR1 is a G-protein coupled receptor activated by proteolytic cleavage. Several studies indicate that thrombin-mediated activation of PAR1 leads to detrimental, pro-inflammatory responses whereas activation by activated protein C (APC) induces anti-inflammatory and cytoprotective signaling. Parmodulin is a small allosteric modulator of PAR1 which activates its cytoprotective signaling. The main aim of my project is to determine the beneficial and detrimental role of PAR1 signaling on vascular complications and to develop a therapeutic intervention to prevent detrimental signaling and preserve beneficial PAR1 signaling in SCD.