Brahma Raju Mopidevi, Ph.D.
Phone: (419) 383-4535
FAX: (419) 383-2871
- B.Sc., Zoology, Botany and Chemistry, 2000, First Class with Distinction from Andhra Loyola College (Autonomous), Vijayawada, India
- M.Sc., Biotechnology, 2002, First Class with Distinction from Andhra University, Andhra Pradesh, India
- Ph.D., Life Sciences (Reproductive Biology) 2008, Devi Ahilya University, Indore, India/Rajiv Gandhi Centre for Biotechnology (RGCB), Trivandrum, India
- Research Scholar (Ph.D.), School of Life Sciences, DAVV Indore/RGCB, Trivandrum, India, 2002-2008
- Postdoctoral Research Associate, Rajiv Gandhi Centre for Biotechnology (RGCB), Trivandrum, India, 2008-2009
- Postdoctoral Fellow, Department of Pathology, New York Medical College, Valhalla, NY, 2009-2011
- Postdoctoral Fellow, Department of Physiology and Pharmacology, University of Toledo, Toledo, OH, 2011-2013
- Assistant Professor, Department of Physiology and Pharmacology, University of Toledo, Toledo, OH, 2013-present
Honors & Awards:
Kidney Council New Investigator Award 2014, Supported by the Council on Kidney in Cardiovascular Disease for the research work entitled "A Genetic Variant of Human Aldosterone Synthase Gene Causes Salt-Dependent High Blood Pressure in Transgenic Mice" in the High Blood Pressure Research (HBPR) Scientific Sessions 2014 held at Hilton San Francisco Union Square, San Francisco, CA, September 9-12, 2014.
Hypertension is a serious risk factor for myocardial infarction, heart failure, vascular disease, stroke, and renal failure. Like other complex diseases, hypertension is caused by a combination of genetic and environmental factors. It has been estimated by segregation analysis and twin studies that approximately 45% of the inter-individual differences in blood pressure can be accounted by genetic differences. However, molecular mechanisms involved in pathophysiology of hypertension are not clear.
Aldosterone synthase, the rate limiting enzyme in the biosynthesis of aldosterone, is encoded by Cyp11B2 gene. This gene is expressed mainly in adrenal cortex and to some extent in kidney, brain, and adipose tissue. The epidemiological studies have suggested that -344T/C polymorphism is shown to be associated with increased aldosterone level and increased blood pressure. The hCyp11B2 gene has 3 SNPs in 1 Kb of its promoter and these polymorphisms are in almost complete linkage dis-equilibirium. These SNPs are rs1799998 (T/C at -344), rs10087214 (C/T at -470), and rs28659182 (C/A at -663). Thus variant -344T almost always occurs with variants -470C and -663A (named haplotype-I), and variant -344C almost always occurs with variants, -470T and -663T (named haplotype-II) in human subjects. In order to understand the physiological role of these haplotypes on transcriptional regulation of hCyp11B2 gene and blood pressure regulation in an in vivo situation, we have generated transgenic mice by knocking in hCyp11B2 gene containing either haplotype-I or haplotype-II at the HPRT locus. Currently our group actively engaged in studying the molecular mechanism by which these promoter polymorphisms alter the binding of the transcription factors and regulate the blood pressure. Further we have extended our research interests to micro RNA and shown that the microRNA miR-31 and miR-584 bind strongly to the human angiotensinogen (hAGT) 3'UTR containing 11525C-allele as compared to 11525A-allele and down-regulate the hAGT mRNA and protein levels in human liver cells. These studies not only provide new insight into understanding the molecular basis of hypertension, but will also have significant clinical relevance to develop new therapeutic strategies for hypertension.
Brahmaraju Mopidevi, Mennakshi Kaw, Nitin Puri, Madhusudan Ponnala, Sudhir Jain, Anita Rana, Narsimha
R. Keetha, Sadik A. Khuder, Steven N. Fiering and Ashok Kumar (2015) Variable transcriptional
regulation of the human aldosterone synthase gene causes salt-dependent high blood
pressure in transgenic mice. Circ Cardiovasc Genet. 8(1):30-39.
Varunkumar G. Pandey, Sudhir Jain, Anita Rana, Nitin Puri, Arudra, S.K., Brahmaraju Mopidevi, Meenakshi Kaw, Alberto Nasjletti and Ashok Kumar (2015) Dexamethasone promotes hypertension by allele-specific regulation of the human antiogensinogen gene. J Biol Chem. 290(9):5749-58.
Shreekrishna Maharjan, Brahmaraju Mopidevi, Meenakshi Kaw, Nitin Puri and Ashok Kumar (2014) Human aldosterone synthase gene polymorphism promotes miRNA binding and regulates gene expression. Physiol Genomics. 46(24):860-865.
Brahmaraju Mopidevi, Madhusudhan Ponnala, and Ashok Kumar (2013) Human angiotensinogen +11525 C/A polymorphism modulates its gene expression through microRNA binding. Physiol Genomics. 45(19):901-906.
Sudhir Jain, Andrej Tillinger, Brahmaraju Mopidevi, Varunkumar G Pandey, Chetankumar K Chauhan, Steven N Fiering, Soren Warming and Ashok Kumar (2010) Transgenic mice with -6A haplotype of the human angiotensinogen gene have increased blood pressure compared with -6G haplotype. The Journal of Biological Chemistry 285(52):41172-86. Epub 2010 Oct 26.
M. Brahmaraju, K.P. Bhagya, Shiny Titus, Arun Sebastian, A.N. Devi, Malini Laloraya and Pradeep G Kumar (2011) AIRE1A might be involved in cyclin B2 degradation in testicular lysates. Biochem Cell Biol. 89(4):411-22.
M. Brahmaraju, Malini Laloraya and Pradeep G Kumar (2009) Review on “Immunodominant sperm antigens and their role in male infertility.” Current Paradigm of Reproductive Immunology, 59-81, ISBN: 978-81-308-0373-9.
Selot R, Kumar V, Shukla S, Chandrakuntal K, Brahmaraju M, Dandin S, Laloraya M and Kumar PG (2007) Identification of a Soluble NADPH Oxidoreductase (BmNOX) with Antiviral Activities in the Gut Juice of Bombyx mori. Biosci Biotechnol Biochem. 71(1):200-205.
M. Brahmaraju, Mohammed Shoeb, Malini Laloraya and Pradeep G. Kumar (2004) Spatio-temporal organization of Vam6P and SNAP on mouse spermatozoa and their involvement in sperm–zona pellucida interactions. Biochemical and Biophysical Research Communications 318(1):148-155.
Sharad Purohit, M. Brahmaraju, Abha Palta, Sunita Shukla, Malini Laloraya and Pradeep G. kumar. (2004) Impaired E-cadherin expression in human spermatozoa in a male factor infertility subset signifies E-cadherin- mediated adhesion mechanisms operative in sperm-oolemma interactions. Biochemical and Biophysical Research Communications 316(3):903-909.