Reena Rao

Assistant Professor of Medicine, Nephrology & Hypertension
Kidney Institute- Faculty
Cancer Center- Faculty
Secondary appointment- Cell and Developmental Biology
Internal Medicine

MSc. Vector Control Research Center, Pondicherry, India
MPhil. Kerala University, India
PhD. Central Food Technological Research Institute, India
Post Doctoral, Vanderbilt University Medical Center


Publications: Click here

Research Focus

Research Focus Glycogen synthase kinase 3 (GSK3) is a multifunctional serine/threonine protein kinase, which has been identified as a putative target for the treatment of disorders including diabetes, ischemic injury, inflammation, cancer, Alzheimer's disease, and bipolar disorders. GSK3 occurs in two isoforms, α and β. Our primary interests are to elucidate the mechanisms by which GSK3 isoforms regulate renal water transport in the kidneys and their role in survival and proliferation of renal tubular cells. We use a combination of in vitro molecular biology techniques, gene knock out mice and in vivo models of disease and development to test our basic findings in renal disease.

1: Regulation of Renal Response to Vasopressin by GSK3

 Regulation of water balance by the kidney is one of the most fundamental homeostatic functions and is rigorously controlled by arginine vasopressin (AVP). High plasma AVP concentrations and disregulated AVP signaling are associated with congestive heart failure, cirrhosis and polycystic kidney disease. Hence, understanding signaling factors that regulate AVP action is important in comprehending such diseases associated with improper water handling. GSK3 could play a crucial role in AVP mediated renal water reabsorption. This view is based on two considerations: 1) lithium, a potent inhibitor of GSK3 causes irreversible and clinically important reduction in maximal urinary concentrating ability, which may lead to nephrogenic diabetes insipidus and 2) our recent findings that GSK3 inhibitors or renal collecting duct specific gene deletion of GSK3ß in mice impaired their urinary concentrating ability in response to water deprivation or AVP analogue treatment. Hence the goal of our studies is to determine the mechanism by which GSK3 regulates AVP signaling in the renal collecting duct and to examine the pathophysiological significance of such regulation in the context of diseases that feature disregulated AVP signaling like polycystic kidney disease and Lithium induced NDI.

 2: Glycogen synthase kinase as a potential drug target in acute kidney injury.

   Acute kidney injury (AKI) characterized by abrupt loss of kidney function is most commonly caused by nephrotoxic or ischemia/reperfusion injury and is generally considered to affect the renal proximal tubules (PT). The mechanisms underlying the complex pathophysiology of AKI involving injury and repair are incompletely understood. GSK3 could be critical in injury and recovery of renal cells following an acute insult since it plays an important role in cell survival, proliferation and epithelial-mesenchymal transition. As a downstream target of PI3 kinase and Wnt signaling, GSK3 could be an important signaling molecule in pathways known to be involved in AKI. Our goal is to examine if GSK3ß plays a crucial role in AKI, and if its inhibition could ameliorate injury and hasten repair in nephrotoxic (HgCl2 induced) ischemia/ reperfusion (I/R) models of AKI in mice.

Last modified: Apr 26, 2013

Contact

Reena Rao
Assistant Professor of Medicine, Nephrology & Hypertension
Kidney Institute- Faculty
Cancer Center- Faculty
Secondary appointment- Cell and Developmental Biology

ID=x3278