Nitin Puri, M.D., Ph.D.
Assistant Professor, Department of Physiology and Pharmacology
Program Director of MSBS-MS
Basic Science Educator & Researcher
- 2005-2010: Ph.D. - New York Medical College, Valhalla, NY - Department of Pharmacology. Advisor: Alberto Nasjletti, M.D.
- 2000-2003: Master of Surgery (Residency Program) - S.S. Medical College, Rewa, M.P, India
- 1994-1999: Bachelor in Medicine, Bachelor in Surgery (M.D) - M.G.M Medical College. Indore, M.P, India
August 2012-present: Assistant Professor, The University of Toledo College of Medicine, Department of Physiology & Pharmacology.
July 2010-August 2011: Postdoctoral fellow, The University of Toledo College of Medicine, Department of Physiology & Pharmacology, (Advisor: Dr. Nader G. Abraham, Professor and Chair, Department of Physiology and Pharmacology, UT Health Science Campus).
August 2005-May 2010: Graduate Student Research Associate, Department of Pharmacology New York Medical College Valhalla NY, (Advisor: Alberto Nasjletti, M.D.).
December 2003-August 2005: Senior Resident Surgeon, B.J.R.M Hospital, Department of Surgery, Jahangirpur B Block, New Delhi, India.
July 2000-July 2003: Resident-General Surgery (Postgraduate residency), Department of Surgery, S.S Medical College & G.M & S.G.M. Hospitals, Rewa M.P., India.
My research interest lies in the investigation of role of redox molecules in the (dys)functional regulation of cardio-vascular and metabolic homeostasis. We also examine the contributions of chronic oxidative stress and metabolic imbalance, as it pertains to the development of obesity and diabetes with associated longterm complications. In this regard, the principal focus of my investigation is the meme-heme oxygenase system. This antioxidant enzyme system is one of the principal cellular defenses against redox imbalance and also plays a central role in cardio-vascular function via its product generation, i.e. carbon monoxide and biliverdin. We have found that chronic oxidative stress has reciprocal effects on HO expression and activity; where a strong transcriptional activation of HO is seen by reactive oxygen species (ROS), emerging evidence shows an inhibitor effect of ROS on HO activity. In this context, we examine the differential cardiovascular and metabolic effects of oxidants, including hydrogen peroxide and superoxide anion, in affecting HO system and examining how this translates to development of a clinical syndrome. Our experimental model systems include resistance arteries, animal models of hypertension (2K1C), animal models of diabetes and metabolic syndrome and in vitro models of human mesenchymal stem cells and mouse pre-adipocytes. Recently, we have shown that cellular overexpression of Sirt1 protects against patho-physiological effects of oxidative stress and are currently exploring the regulatory crosstalk between HO system and Sirt1 & 6. An equally exciting focus my research entails examining HO-dependent regulation of eicosanoids and their physiological effects, particularly in the vasculature and perivascular adipocytes. We have made significant headway in this direction where we have shown existence of a feedback loop between epoxides and HO whose stimulation by either of the two systems attenuates oxidative stress and adipocyte dysfunction in in vitro as well as in vivo models.
2011: Outstanding (Second Place) oral presentation in Molecular and Genetic Basis of Hypertension at the 2011-Experimental Biology meeting, Washington D.C. Travel award granted.
2011: Outstanding poster award at the 13th International Winter Eicosanoids Conference, Baltimore, MD.
2010: Martha Lucas Pate, Ph.D., Memorial Award, "In recognition of academic excellence and leadership in social and humane concerns in medicine, science or health." The Trustees of New York Medical College, New York, NY.
1. Puri N, Zhang F, Monu SR, Sodhi K, Bellner L, Lamon BD, Zhang Y, Abraham NG, Nasijletti A. Antioxidants condition pleiotropic vascular responses to exogenouse H(2)O(2): role of modulation of vascular TP receptors and the heme oxygenase system. Antioxid Redox Signal. 2013 Feb 10;18(5):471-480. doi: 10.1089/ars.2012.4587. Epub 2012 Sep 28.
2. Cao J, Vecoli C, Neglia D, Tavazzi B, Lazzarino G, Novelli M, Masiello P, Want YT, Puri N, Paolocci N, L'abbate A, Abraham NG. Cobalt-rotoporphyrin improves heart function by blunting oxidative stress and restoring NO synthase equilibrium in an animal model of experimental diabetes. Front Physiol. 2012; 3:160. doi: 10.3389/fphys.2012.00160. Epub 2012 Jun 4.
3. Cao J, Puri N, Sodhi K, Bellner L, Abraham NG, Kappas A. Apo A1 mimetic rescues the diabetic phenotype of HO-2 knockout mice via an increase in HO-1 adiponectin and LKBI signaling pathway. Int J Hypertens. 2012;2012:628147. doi: 10.1155/2012/628147. Epub 2012 Apr 4.
4. Puri N, Sodhi K, Haarstad M, Kim DH, Bohinc S, Foglio E, Favero G, Abraham NG. Heme induced oxidative stress attenuates sirtuin1 and enhances adipogenesis in mesenchymal stem cells and mouse pre-adipocytes. J Cell Biochem. 2012 Jun;113(6):1926-35. doi: 10.1002/jcb.24061.
5. Sodhi K*, Puri N*, Inoue K, Falck JR, Schwartzman ML, Abraham NG. EET agonist prevents adiposity and vascular dysfunction in rats fed a high fat diet via a decrease in Bach 1 and an increase in HO-1 levels. Prostaglandins Other Lipid Mediat. 2012 Aug; 98(3-4):133-42. doi: 10.1016/ j.prostaglandins. 2011.12.004. Epub 2011 Dec 24. *contributed equally to this work.
6. Cao J, Sodhi K, Puri N, Monu SR, Rezzani R, Abraham NG. High fat diet enhances cardiac abnormalities in SHR rats: Protective role of heme oxygenase-adiponectin axis. Diabetol Metab Syndr. 2011 Dec 23; 3(1):37. doi: 10.1186/1758-5996-3-37.
7. Cao J, Inoue K, Sodhi K, Puri N, Peterson SJ, Rezzani R, Abraham NG. High-fat diet exacerbates renal dysfunction in SHR: reversal by induction of HO-1-adiponectin
axis. Obesity (Silver Spring). 2012 May;20(5):945-53. doi: 10.1038/oby.2011.365. Epub 2011 Dec 22.
8. Kawakami T, Puri N, Sodhi K, Bellner L, Takahashi T, Morita K, Rezzani R, Oury TD, Abraham NG. Reciprocal effects of oxidative stress on heme oxygenase expression and activity contributes to reno-vascular abnormalities in EC-SOD knockout mice. Int J Hypertens. Vol. 2012;2012:740203. doi: 10.1155/2012/740203. Epub 2012 Jan 12.