Physiology and Pharmacology

Sudhir Jain, Ph.D.


 Assistant Professor

 Phone: 419-383-4130
 Fax:     419-383-2871


  • 1989, B.Sc. (Zoology, Chemistry, Environmental Science), Delhi University, Delhi, India
  • 1991, M.Sc., (Zoology), Sagar University, Sagar, India
  • 1997, Ph.D., Life Sciences (Reproductive Biology) Devi Ahilya University, Indore, India

  • Research Scholar (Ph.D.), 1992-1997, School of Life Sciences, DAVV, Indore, India
  • Postdoctoral Research Associate, 1997-1999, National Institute of Immunology, Delhi, India.
  • Postdoctoral Fellow, January 2000-October 2000, Animal Science Department, Rutgers University, New Brunswick, New Jersey.
  • Postdoctoral Associate, October 2000-December 2003, New York Medical College, Valhalla, New York.
  • Research Assistant Professor, January 2004-September 2011), New York Medical College, Valhalla, New York.
  • Assistant Professor, October 2011-present, University of Toledo, Toledo, Ohio.

Research Interest

Transcriptional regulation of genes associated with Human Hypertension

My current research interest is to understand molecular mechanisms involved in hypertension and hypertrophy with special emphasis on the role of the renin-angiotensin system (RAS) which plays an important role in the regulation of blood pressure.  The Octapeptide Angiotensin-II is one of the most potent vaso-active substances known and is synthesized from its precursor molecule, antiotensinogen, which is primarily synthesized in the liver and to a lesser extent, in the kidney, brain, heart, adrenal, fat and vascularwalls by the combined proteolytic action of renin and angiotensin converting enzyme.  Recent studies have shown that patients with essential hypertension have higher plasma angiotensinogen levels and linkage studies have confirmed a direct relationship between angiotensinogen gene and essential hypertension.  However, molecular mechanisms involved in this process are not known.  In addition, molecular mechanisms involved in tissue and hormone specific expression of this gene remain to be identified.  In order to understand the mechanisms involved in its transcriptional regulation, we have constructed expression vectors where different deletions in the 5'-flanking sequence of the human angiotensinogen gene (5' untranslated region containing the promoter) are fused to the reported luciferase gene. Transient transfection of these expression vectors, combined with DNAase footprinting and gel mobility shift assay, have identified cis-acting DNA elements that are involved in the regulation of angiotensinogen gene expression in the cell lines from liver, brain, kidney and adipocytes.  The human angiotensinogen gene contains various polymorphic sites (SNP) in its promoter.  We have analyzed SNPs at -6, -20, -217, -532, -777, -793, -1074, -1564, -1565, -1679 positions in human AGT gene promoter.  We have identified transcription factors that bind to these sites.  Our hyposhesis is that increased expression of the angiotensinogen gene as a result of differential binding of the identified transcription factors with these polymorphic sites may result in increased blood pressure in these patients.  We are now using transgenic animals containing human angiotensinogen gene with different polymorphic sites to study the role of these polymorphisms in an in-vivo situation.

Representative papers published in international journals

  • Sudhir Jain, Andrej Tillinger, Brahmaraju Mopidevi, Varunkumar G Pandey, Chetan KC Chauhan, Steven Fiering, Soren Warming and Ashok Kumar (2010). Transgenic mice with -6A haplotype of the human angiotensinogen gene have increased blood pressure compared to -6G haplotype. The Journal of Biological Chemistry 285:41172-41186.
  • Sudhir Jain, Govindaiah Vinukonda, Steven Fiering, Ashok Kumar (2008). A haplotype o f human angiotensinogen gene containing -217A increases blood pressure in transgenic mice as compared to – 217G. American Journal of Physiology-Regulatory Integrative Comp Physiol. 295:1849-1857. 
  • Sudhir Jain, Yana li, Sai Patil, Ashok Kumar (2007). HNF-1α plays an important role in IL-6 induced expression of the human angiotensinogen gene. American Journal of Physiology-Cell Physiology. 293:C401-C410 (Corresponding Author: SUDHIR JAIN).
  • Sudhir Jain, Mehul Shah, Yanna Li, Govind Vinukonda, Pravin B Sehgal, Ashok Kumar (2006). Interferon-γ increases the expression of Human Angiotensinogen Gene. BBA-Gene Structure and Expression, 1759, 340-347.
  • YanaLi, Sudhir Jain, Sai Patil, Ashok Kumar (2006). A haplotype of angiotensinogen gene is associated with essential hypertension and effects promoter activity in adipocytes. Vascular Pharmacology, 44, 29-33.
  • Jain S, Li Y, Kumar A, Sehgal PB (2005). Transcriptional signaling from membrane raft-associated glucocorticoid receptor (GR). Biochem. Biophys. Res. Commun., 336 (1) 3-8.
  • Ashok Kumar, Yanna Li, Sai Patil, Sudhir Jain (2005). A haplotype of the angiotensinogen geneis associated with hypertension in African-Americans. Clinical and Experimental Pharmacology and Physiology, 32, 495-502.
  • Sudhir Jain, Yana Li, Sai Patil, Ashok Kumar (2005). A SNP in hAGT gene is associated with essential hypertension and effects glucocorticoid induced promoter activity. Journal of Molecular Medicine (JMM), 83(2):121-135.
  • Sudhir Jain, Xiangna Tang, Chittampalli S. Narayanan, Yogesh Aggarwal, Stephen M Peterson, Clinton D Brown, Jurg Ott, and Ashok Kumar (2002). Angiotensinogen gene polymorphism at -217 affects basal promoter activity and is associated with hypertension in african American. The Journal of Biological Chemistry, 277(39):36889-36896.
  • P. Das, G. Tiwari, S. Jain and LC Garg (2000). Rapid Communication: Nucleotide sequence of the river buffalo beta-casein cDNA. J Animal Sciences , 78(5):1390.
  • P Das, S. Jain, G. Tiwari and LC Garg (2000).Rapid Communication : Nucleotide sequence of the river buffalo kappa-casein cDNA . J Animal Sciences , 78(5):1389.
  • Jain S, Saxena D, Kumar GP, and Laloraya M. (2000). NADPH dependent superoxide generation in the ovary and uterus of mice during estrous cycle and early pregnancy. Life Sciences, 66(12):1139-1146.




Last Updated: 6/26/15