Associate Professor, UNMC Department of Biochemistry and Molecular Biology
Ph.D, Banaras Hindu University
“Molecular mechanisms of mucosal Inflammation and associated cancer; and Ciliogenesis, autophagy and renal diseases”
Research Opportunities in my laboratory:
Understanding the causal role of the epithelial barrier in the regulation of mucosal inflammation and associated cancer: One of the research focuses of my laboratory is to understand the molecular details of the processes that regulate mucosal antigen-immune interaction, inflammation and progression to colitis-associated cancer. In this regard, we focus upon the role of the mucosal epithelial barrier, as a single layer of epithelium helps maintain the separation between the luminal antigens and the mucosal immune components. In accordance, leakiness of this barrier often associates with Inflammatory Bowel Disease (IBD), a conglomerate of auto-immune disorders characterized by recurring inflammation of the colon and small intestine. However, recent studies including ours have suggested that the role of the mucosal barrier in the regulation of immune homeostasis and inflammation is rather complex and dynamic, and the outcome may vary depending upon the timing and the extent of leakiness. We are using multiple mouse models manipulated for the proteins critical in the regulation of mucosal barrier function to study the molecular details of the role of the intestinal epithelial barrier function in the regulation of intestinal inflammation. We are also studying the potential cross-talk and interdependence between the immune components and the epithelium to determine how mucosal inflammation promotes colon cancer.
Regulation of renal tubular epithelial cell morphogenesis and renal cancer: These studies are aimed at understanding the cross-talk between the EGF receptor (EGFR) and the cell-cell adhesion moiety especially the tight junction components in the regulation of renal epithelial cell morphogenesis, its role in renal injury and repair, and dysregulation during renal diseases including renal cancer. Here, we examine the cross-talk between the cellular components regulating epithelial differentiation, stress-response and cell-division, and their causal association with EGFR activation. We use three-dimensional cell culture models and genetically engineered mouse models to test our hypothesis.