Xiao Li, MD

Associate Professor

School of Medicine
Department
Physiology
Xiao Li

Education & Affiliations

MD: Guangxi Medical University, Nanning, China (1983)
MSc: Department of Pharmacology, Monash University, Melbourne, Australia (1995)
Postdoctoral Training: Department of Pharmacology, Monash University, Melbourne, Australia (1996-2000)
Postdoctoral Training: Research Fellow, Department of Pharmacology, University of Michigan, Ann Arbor, Michigan, MI (2002-2003)

Areas of Expertise

Genetic mechanisms of hypertension
Renal physiology and kidney disease
Renin Angiotensin System

Biography

Dr. Li is currently a Research Associate Professor in the Department of Physiology and the Tulane Hypertension and Renal Center of Excellence at Tulane University School of Medicine. She joined Tulane University from the Department of Pharmacology and Toxicology at the University of Mississippi Medical Center in Jackson, Mississippi, where she was a Senior Research Scientist. Dr. Li graduated with a medical degree (equivalent to M.D. in the USA) from Guangxi Medical University, Nanning, China in 1983, and with a research Master of Science (M.Sc.) degree in Cardiovascular Pharmacology from the Department of Pharmacology at Monash University in Melbourne, Australia in 1996, where Dr. Li studied the cardiovascular pharmacology of nonpeptide angiotensin II receptor antagonists and their pharmacological effects on regional hemodynamics, including their antihypertensive actions, renal, mesenteric, and hindquarter vascular resistance and compliances. She undertook further postdoctoral training in genomic and molecular pharmacology as a Research fellow in the Department of Pharmacology at the University of Michigan, Ann Arbor from 2002-2003. Dr. Li was subsequently appointed to an Assistant Staff Investigator in the Division of Hypertension and Vascular Research at Henry Ford Hospital, focusing on studying on the novel roles of circulating (endocrine or tissue-to-tissue), paracrine (cell-to-cell), and intracrine (intracellular) angiotensin II and its receptor signaling transduction mechanisms in the development of hypertension and kidney injury from 2004 to 2010. She moved to the Department of Pharmacology and Toxicology at the University of Mississippi Medical Center in 2010 and worked as a Senior Scientist on the roles of circulating, paracrine, and intracrine angiotensin II in the regulation of blood pressure and proximal tubular function using novel cultured proximal tubule cells and transgenic mutant mouse models. Dr. Li has published 53 high impact articles with 6 original articles being selected for an editorial commentary, 3 for highlighting on a journal’s color cover, 2 for Innovative Methodology articles, 2 for recommendation by the Faculty of 1000, and 3 as a journal’s featured article in this research field. Over her research career, she has been recognized by an Australian Academy of Science Young Investigator Travel Award, Glasgow, International Society of Hypertension (1996); New Investigator Award at the 59th Annual Fall Conference and Scientific Sessions of the Council for High Blood Pressure Research, New Investigator Award at the 62nd Annual Fall Conference and Scientific Sessions of the Council for High Blood Pressure Research, and the Kidney Council New Investigator Award at the 63rd Annual Fall Conference and Scientific Sessions of the Council for High Blood Pressure Research, respectively. Dr. Li’s research is currently supported by grants from National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK).  

Research

As a Senior Co-Investigator, Dr. Li 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 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, Dr. Li 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

Contributions

  1. Li XC and Zhuo JL. Phosphoproteomic analysis of AT1 receptor-mediated signaling responses in proximal tubules of angiotensin II-induced hypertensive rats. Kidney Int. 80(6): 620-632, 2011
  2. Li XC, Zhuo JL. Proximal tubule-dominant transfer of AT1a receptors induces blood pressure responses to intracellular angiotensin II in AT1a receptor-deficient mice. Am J Physiol Regul Integr Comp Physiol. 304(8):R588-98, 2013. 
  3. 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. 
  4. 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. 
  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. 

Publications for Dr. Xiao Li.