Nagesha Guthalu Kondegowda, Ph.D.
2004, Ph.D., Biotechnology, Central Food Technological Research Institute/University of Mysore, Mysore, India
1996, M.Sc., Biochemistry, University of Mysore, Mysore, India
1994, B.Sc., Botany, Biochemistry, Microbiology, University of Mysore, Mysore, India
2000-2003, Senior Research Fellow, Council of Scientific and Industrial Research, India
2004-2005, Visiting Scientist, Immunomodulation Research Centre, University of Ulsan, Ulsan, South Korea
2005-2007, Postdoctoral Research Associate, Virginia Tech, Blacksburg, Virginia
2007-2011, Postdoctoral Research Associate, University of Pittsburgh, Pittsburgh
2018-present, Assistant Research Professor, Department of Translational Research &Cellular Therapeutics, City of Hope, Duarte, California
2013-2018, Assistant Professor (Research), Diabetes Obesity and Metabolism Institute, Icahn School of Medicine at Mount Sinai, New York
2011-2013, Research Associate, University of Pittsburgh, Pittsburgh
Effect of PTHrP and an FDA-approved cell cycle inhibitor drug on beta cell homeostasis:
Effect of lactogens on beta cell survival:Lactogenic hormones, such as prolactin and placental lactogen act by binding to a common receptor, the prolactin receptor, are indispensable in facilitating the normal growth and function of the beta cell during development and during pregnancy, as demonstrated by various studies. Though many studies have demonstrated that these hormones can induce proliferation and enhance function of beta cells, their effect on beta cell survival was not known. Based on the effects of these hormones in other cell types, we hypothesized that they would protect beta cells from cell death inducers. Indeed our work has demonstrated that these hormones protect rodent and human beta cells against varied cell death inducers relevant to the pathophysiology of type 1 and type 2 diabetes. We have also shown the importance of the downstream JAK2/STAT5 pathway and the anti-apoptotic molecule BclXL for mediating the prosurvival effects of these hormones in rodent and human beta cells. Our recent findings also demonstrated the protective effect of lactogens against endoplasmic reticulum stress (ER stress) induced rodent and human beta cell death and prevents diabetes incidence in Akita mice. Further, our yet unpublished research demonstrates that prolactin treatment in NOD-Ltj mice, a type 1 diabetic rodent model, not only prevents but also reverses recent onset type 1 diabetes.
Osteoprotegerin effect on beta cell homeostasis:Our quest to find the downstream targets of lactogenic hormones led to a recent finding that the bone-related peptide, osteoprotegerin (OPG) is induced by lactogens in beta cells. We showed that OPG, besides mediating lactogen-induced beta cell proliferation, can also enhance rodent beta cell proliferation in vivo in young and aged mice. Furthermore, OPG has proliferative and pro-survival effects on human beta cells. Being a soluble decoy receptor, OPG acts by inhibiting the RANKL/RANK or the TRAIL/DR pathways. Our studies have found that the proliferative effect of OPG in rodent and human beta cells is mediated through inhibition of the RANKL/RANK pathway. We have used these findings to examine the potential of repurposing an FDA-approved osteoporosis drug, Denosumab, which is a RANKL antibody, on human beta cell proliferation and survival, for the treatment of diabetes. Currently we are studying the physiological, mechanistic, and therapeutic aspects of these molecules and pathways in the beta cell. We have two patents on the role of OPG in beta cell proliferation and survival.
2013, Training Travel Award Supplement from JDRF
2012, Midwest Islet Club Meeting, Travel Award
2010, 92nd Endocrine Society Meeting, Travel Award