Kailash N. Pandey, PhD

Professor, Department of Physiology

Tulane Cancer Center Member - Cancer Biology Research Program
Phone
504-988-1628
Office Address
1430 Tulane Avenue, 4th Floor, Room 4022, New Orleans, LA 70112
School of Medicine
Physiology
Tulane Center Aging
Tulane Cancer Center
Debakey
TIPS Mentor
Kailash N Pandey

Education & Affiliations

PhD: University of Kentucky (1979)
Postdoctoral Training: Vanderbilt University, Department of Biochemistry, Nashville, TN (1981-1985)

Areas of Expertise

Molecular basis of hypertension
Atrial natriuretic peptides and receptors
Renin and angiotensin
Cardiovascular dysfunction
Gene regulation and genomics

Biography

Dr. Kailash Nath Pandey received his Bachelors from Agra university and Master's degree from Kanpur University, 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 Research Instructor and in 1987 was promoted to Research Assistant Professor. In 1990 he joined 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 a Professor and Vice Chair of Medical Research in Physiology. He has received several grants from AHA, including an Established Investigatorship award and continuous multiple NIH grants to study the atrial and brain natriuretic peptides (ANP, BNP) and their cognate membrane guanylyl cyclase-A/natriuretic peptide receptor-A (GC-A/NPRA) in recombinant cells in vitro and genetically altered animal models in vivo.  He has served on the Editorial Board of 14 journals, including Endocrinology, Physiological Genomics, and Hypertension and on the study section of AHA, NIH and NSF grant review committees. He has received numerous awards and honors, including Lewis K. Dahl Award from the AHA-Council on Hypertension and Hans-Peter Krayenbuehl award from Int. Academy of Cardiology.  He is a member of several societies, including AHA, ASH, APS, ASN, ASBMB, and Endocrinology.  The long-term objectives of his research projects are to delineate the molecular basis of natriuretic peptides and their receptor in the regulation of blood pressure and renal and cardiovascular homeostasis.

Research

The primary goal of our research is to determine the genetic and epigenetic 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 ANP and BNP that control blood pressure and renal and cardiovascular disorders.  Our research has focused on the regulatory action of ANP and BNP that is mediated by interacting with membrane GC-A/NPRA, which synthesizes the intracellular second messenger cGMP and plays the pivotal role in the regulation of hypertension and hypertensive heart disease. Click here to look at photos of lab personnel.  

Contributions

  1.  Khurana, M.L., Mani, I., Kumar, P., Ramasamy, C., and Pandey, K.N. Ligand-dependent downregulation of guanylyl cyclase/natriuretic peptide receptor-A: Role of miR-128 and miR-195. Int. J. Mol. Sci. 23:1338 (2022).
  2. Subramanian, U., Ramasamy, C., Samivel, R., Oakes, J.M., Gardner, J.D., and Pandey, K.N. Genetic disruption of guanylyl cyclase/natriuretic peptide receptor-A triggers differential cardiac disorders in male and female mutant mice: Role of TGF-β1/SMAD signaling pathways. Int. J. Mol. Sci. 23(19):11487 (2022). 
  3. Das, S., Neelamegam, K., Peters, W.N., Periyasamy, R., and Pandey. K.N. Depletion of cyclic-GMP levels and inhibition of cGMP-dependent protein kinase activate p21Cip1/p27Kip1 pathways and lead to renal fibrosis and dysfunction. The FESAB Journal. 34:11925-11943 (2020).
  4. Arise, K.K., Kumar, P., Garg, R., Samivel, R., Zhao, H, Pandya, K., Nguyen, C., Lindsey, H., and Pandey, K.N. Angiotensin II- represses Npr1 gene expression and receptor function by recruitment of transcription factors CREB and HS-4a.and activation of HDACs. Scientific Reports. 10:4337-4354 (2020).
  5. Mani, I. and Pandey, K.N. Emerging concepts of receptor endocytosis and concurrent intracellular signaling:  Mechanisms of guanylyl cyclase/natriuretic peptide receptor- A activation and trafficking. Cellular Signaling, 60: 17-30 (2019).
  6. 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).
  7. 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-F 795 (2017). 
  8. Sen, A., Kumar, P., Garg, R., Lindsey, S.H., Katakam, P.V.G., M. Bloodworth, and Pandey, K.N. Transforming growth factor-beta1 antagonizes the transcription, expression, and vascular signaling   of guanylyl cyclase/natriuretic peptide receptor-A gene: Role of δ EF-1. FEBS J., 283: 1767-1781 (2016). 
  9. 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 Reports, 35 (article: e0026): 1-17 (2015). 
  10. 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).

PubMed listing for Kailash N. Pandey, PhD