PhD: University of Kentucky (1979)
Postdoctoral Training: Vanderbilt University, Department of Biochemistry, Nashville, TN (1981-1985)
Dr. Kailash Nath Pandey received his Bachelors and Master's degrees in Kanpur, India. He received his PhD in Cell Biology from the University of Kentucky in 1979. He carried out postdoctoral studies in the Department of Biochemistry at Vanderbilt University and in 1986 he was appointed as a faculty member. In 1990 he joined the faculty of the Medical College of Georgia as an Associate Professor in the Department of Biochemistry and Molecular Biology. Dr. Pandey joined Tulane in 1997 where he is Professor and Vice Chair of Medical Research in Physiology. He has received several grants from AHA, including an Established Investigatorship award and continuous multiple grants from the NIH/NHLBI and NIH/NICHD. He has served on the Editorial Board of 14 journals and on the study section of AHA, NIH and NSF grant review committees. He has received numerous awards and honors and is a member of several societies, including APS, ASBMB, AHA, ASH and Endocrinology. The long-term objectives of his research projects are to delineate the molecular and physiological basis of atrial and brain natriuretic peptides (ANP, BNP) and their receptors, which regulate blood pressure and cardiovascular homeostasis.
The primary goal of our research is to determine the genetic and molecular basis of hypertension and cardiovascular disorders in age- and sex-dependent manner. The long-term objectives of our research projects are to determine the molecular and cellular action of atrial and brain natriuretic peptides (ANP, BNP) that control blood pressure and cardiovascular homeostasis. Our research has focused on the regulatory action of ANP and BNP that is mediated by interacting with guanylyl cyclase/ natriuretic peptide receptor-A (GC-A/NPRA) which synthesizes the intracellular second messenger cGMP and plays a central role in the pathophysiology of hypertension and cardiovascular disorders. We hope to learn the structural components of the receptor that might be critical for the hormone-dependent signaling process in model cell lines and Npr1 (coding for GC-A/NPRA) gene-targeted (gene-knockout and gene-duplication) mutant mice both globally and in the cell-specific manner in vivo. Our studies are also aimed to test directly the efficacy of Npr1 transcriptional regulatory elements, and the impact of Npr1 gene dosage and null mutation in the regulation of blood pressure and cardiovascular disorders at the molecular level.
Prerna Kumar, PhD – Research Instructor
Kandasamy Neelamegam, PhD- Postdoctoral Research Fellow
Chandramohan Ramasamy, PhD – Postdoctoral Research Fellow
Helene Chen, BS – Medical Student
Brooke Beasley, BS - Masters Student
Valeria Noguera, MS – Laboratory Volunteer
- Vellaichamy, V., Das, S., Subramanian, U., Maeda, N., and Pandey, K.N. Genetically altered mouse models of guanylyl cyclase/natriuretic peptide receptor-A exhibit cardiac expression of pro-inflammatory mediators in a gene-dose-dependent manner. Endocrinology, 155:1045-1056 (2014).
- Kumar, P., Tripathi, S., and Pandey, K.N. Histone deacetylase inhibitors modulate the transcriptional regulation of guanylyl cyclase/natriuretic peptide receptor-A: Interactive roles of modified histones, histone acetyltransferase, p300, and SP-1. J. Biol. Chem. 289:6991-7002 (2014).
- Mani, I., Garg, R., S. Tripathi, and Pandey, K.N. Subcellular trafficking of guanylyl cyclase/natriuretic peptide/receptor-A with concurrent generation of intracellular cGMP. Bioscience Report, 35(article: e0026): 1-17 (2015).
- Sen, A., Kumar, P., Garg, R., Lindsey, S.H., Katakam, P.V.G., M. Bloodworth, and Pandey, K.N. Transforming growth factor-b1 antagonizes the transcription, expression, and vascular signaling of guanylyl cyclase/ natriuretic peptide receptor-A gene by TGF-β1: Role of δ EF-1. FEBS J., 283: 1767-1781 (2016).
- Kumar, P., Gogulamudi, V.R., Periyasamy, R., Raghavaraju, G., Subramanian, U., and Pandey, K.N. Inhibition of HDAC enhances STAT acetylation, blocks NF-kB, and suppresses the renal inflammation and fibrosis in Npr1 haplotype male mice. Am. J. Physiol. Renal Physiol. 313: F781-F795 (2017).
- Gogulamudi, V.R., Mani, I., Subramanian, U., and Pandey, K.N. Targeted disruption of Npr1 causes the depletion of T regulatory cells and provokes high levels of proinflammatory cytokines in the kidneys of female mutant mice. Am. J. Physiol. Renal Physiol. 316: F1254-F1272 (2019).
- Arise, K.K., Kumar, P., Garg, R., Samivel, R., Zhao, H, Pandya, K., Nguyen, C., Lindsey, S., and Pandey, K.N. Angiotensin II- represses Npr1gene expression and receptor function by recruitment of transcription factors CREB and HS-4a.and activation of HDACs. Scientific Reports, 10: 4337-4353 (2020).
PubMed listing for Kailash N. Pandey, PhD