Jia 'Joe' Zhuo, MD, PhD

Director, Tulane Hypertension & Renal Center of Excellence (THRCE)

Professor
Phone
(504) 988-4363
School of Medicine
Department
Joe Zhuo

Education & Affiliations

MD: Guangxi Medical University, Nanning, China (1983)
PhD: University of Melbourne, Melbourne, Australia (1990)
Postdoctoral Training: National Health and Medical Research Council (NH&MRC) of Australia Research Officer, Department of Medicine, Austin & Repatriation Medical Center, University of Melbourne, Melbourne, Australia (1990-1992)
Postdoctoral Training: NH&MRC Senior Research Officer, Department of Medicine, Austin & Repatriation Medical Center, University of Melbourne, Melbourne, Australia (1993-1996)
Sabbatical Faculty Research: Visiting Assistant Professor, Department of Physiology, Tulane University School of Medicine, New Orleans, LA (1999-2000)

Areas of Expertise

Hypertension
Renin Angiotensin System
G Protein-coupled receptor pharmacology

Biography

Dr. Zhuo is a Professor of Physiology in the Departments of Physiology and the Director of Tulane Hypertension and Renal Center of Excellence (THRCE) at Tulane University School of Medicine, New Orleans, Louisiana. He joined Tulane University School of Medicine from the University of Mississippi Medical Center, where he served as a tenured professor and the Director of Receptor and Signal Transduction Laboratory in the Department of Pharmacology and Toxicology. Dr. Zhuo received a Doctor of Medicine degree (M.D.) from Guangxi Medical University, Nanning, China in 1983, and a Ph.D. degree in renal physiology and hypertension from the Department of Physiology at the University of Melbourne, Victoria, Australia in 1990. He served as a National Health and Medical Research Council of Australia Senior Research Officer at the Austin and Repatriation Medical Center and Howard Florey Institute of Experimental Physiology and Medicine at the University of Melbourne from 1993 to 2000, and a Senior Staff Investigator in the Hypertension and Vascular Research Division at Henry Ford Hospital, Detroit, Michigan from 2001 to 2010. Dr. Zhuo has 30 years’ sponsored research investigating the roles of circulating (endocrine), tissue (paracrine), and intracellular (intracrine) angiotensin II and its receptor mapping and signaling mechanisms in renal physiology and hypertension. His research has been continuously supported by grants from the National Health and Medical Research Council (NH&MRC) of Australia, American Heart Association (AHA), American Society of Nephrology (ASN), and National Institute of Health (NIH). As one of the renowned experts in the intratubular renin-angiotensin research field, Dr. Zhuo is a regular invited national and international speaker; and has published over 115 peer-reviewed journal articles and book chapters. He is an elected Fellow of the American Association for the Advancement of Science (FAAAS), Section on Medical Sciences, Overseas Fellow of Royal Society of Medicine (FRSM), England, and a Fellow of American Heart Association (FAHA) and American Society of Nephrology (FASN), respectively. Dr. Zhuo was the past Chair of the American Physiological Society (APS) Physiological Genomics Group, a permanent member for NIH/Center for Scientific Review Hypertension and Microcirculation Study Section, and Ad Hoc reviewer for NH&MRC of Australia, Chinese Ministry of Education, and Danish Council for Independent Research. His research is currently supported by several grants from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK).

Research

Dr. Zhuo’s laboratory is interested in studying the roles of endocrine (tissue-to-tissue), paracrine (cell-to-cell), and intracrine (endosomal, mitochondrial and nuclear) angiotensin II (ANG II) and its G protein-coupled receptor (GPCR) signal mechanisms in the proximal tubules of the kidney and blood pressure control. Supported by several grants from the NIDDK, the laboratory currently investigates: 1) the molecular and signaling mechanisms by which circulating and paracrine ANG II is taken up by the proximal tubule of the kidney to act as an intracellular peptide; 2) high resolution confocal and electron microscopic autoradiographic localization of the internalized ANG II and its receptors in intracellular organelles including endosomes, mitochondria and nucleus; 3) the effects and signaling mechanisms by which intracellular ANG II induces long-term genomic or transcriptional effects; 4) the role of the sodium and hydrogen exchanger 3 (NHE3) in the proximal tubule of the kidney on pressure natriuresis and blood pressure responses to paracrine and intracellular ANG II; and 5) the role and signaling mechanisms of proximal tubule ANG II and AT1a receptors in the pathogenesis of renal ischemia and reperfusion injury and kidney diseases.  

To test the hypotheses, the laboratory uses complementary innovative and state of the art approaches including: 1) live cell confocal fluorescent imaging; 2) high resolution electron microscopic autoradiography and immunohistochemistry; 3) intravital multi-photon functional imaging; 4) proximal tubule cells derived from human kidney, wild-type, AT1a (AT1a-KO) and AT2 receptor-deficient mice (AT2-KO); 5) novel mouse models with proximal tubule-specific knockout of angiotensinogen (PT-AGT-KO), AT1a (PT-AT1a-KO), AT2 (PT-AT2-KO), NPRA receptors (PT-NPRA-KO), NHE3 (PT-NHE3-KO), and SIRT3 (PT-SIRT3-KO); 6) proximal tubule-specific, mitochondria- or nucleus-targeting overexpression of an intracellular cyan fluorescent fusion of ANG II protein (mito- or NLS-ECFP/ANG II) or AT2 receptors (mito-AT2R/GFP); and 7) real-time RT-PCR, gene microarrays, proteomics and Western blot analyses. The new knowledge generated from these studies may lead to the shift of current renin-angiotensin paradigms and aid the development of new classes of multifunctional drugs to treat ANG II-dependent or other hypertension with target organ injury by blocking not only endocrine and paracrine, but also intracellular or nuclear actions of ANG II, or by promoting the pressure natriuresis response through the inhibition of proximal tubule NHE3 in the kidney.  

Lab Members:

  • Jia Long (Joe) Zhuo, M.D., Ph.D., Professor & Director
  • Xiao Chun Li, M.D., M.Sc., Associate professor
  • Mohammed Haque, Ph.D., Instructor
  • Ana Paula Leite, Ph.D., Postdoctoral Fellow
  • Liang Zhang, M.D., Ph.D., Visiting Scholar
  • Nina Majid, B.S., Senior Program Coordinator

Collaborators:

  • Bruce A. Molitoris, M.D., Professor of Medicine, Indiana University School of Medicine
  • Jian-Xiong Chen, M.D., Professor, The University of Mississippi Medical Center
  • Xinchun Zhou, M.D., Ph.D., Associate Professor, The University of Mississippi Medical Center
  • Drazen Raucher, Ph.D., Professor, The University of Mississippi Medical Center

Publications

  1. Li XC, Zhu DM, Zhang JF, Zhuo JL. Intratubular and intracellular renin-angiotensin system in the kidney: a unifying perspective in blood pressure control. Clin Sci (Lond); 132(13):1383-1401, 2018. PMID: 29986878
  2. Zhuo JL and Li XC. De Novo DNA (de)methylation in the kidney: an epigenetic mechanism and a potential target for salt-sensitive hypertension. Hypertension 72:1084-1086, 2018. PMID: 30354833
  3. Li XC, Zhu DM, Soleimani M, Rubera I, Michel R, Zhang JF, Zhuo JL. Proximal tubule-specific deletion of the Na+/H+ exchanger 3 promotes the pressure natriuresis response and lowers blood pressure in mice. Hypertension 72(6):1328-1336, 2018. PMID: 30571224
  4. Zhuo JL, Li XC. Angiotensin III/AT2 receptor/NHE3 signaling pathway in the proximal tubules of the kidney: a novel natriuretic and antihypertensive mechanism in hypertension. Journal of American Heart Association (JAHA) 8(9):e012644, 2019. PMID: 31039655
  5. Li XC, Zhang JF, Soleimani M, Rubera I, Michel R, Zhuo JL. Proximal tubule-selective deletion of the Na+/H+ exchanger 3 attenuates angiotensin II-induced hypertension in mice. Hypertension, 2019;74(3):526-535. doi: 10.1161/HYPERTENSIONAHA.119.13094.

Publications for Dr. Jia 'Joe' Zhuo.