Xiang-An Li, Ph.D.
Associate Professor
Department of Pediatrics
MIDS 401B
Department of Pediatrics
725 Rose Street, Lexington, KY 40536
Tel: 859-257-5113; email:
xli2@email.uky.edu
Academic Appointments:
Publication Listings on PubMed
• Department of Pediatrics, College of Medicine
• Graduate Center for Nutritional Sciences
Education:
• B.S., Shandong University, Shandong, China.
• M.S., Shandong University, Shandong, China
• Ph.D., Osaka University School of Medicine
Awards:
Sasakawa Medical Scholarship
China Outstanding Young Teacher Award
Wethington Award for Excellence in Research
Irvine H. Page Young Investigator Award
Specific Interest in Nutrition:
Diet in atherosclerosis and sepsis
Research
My laboratory focuses on the roles of scavenger receptor BI (SR-BI) in inflammatory diseases including sepsis, atherosclerosis, and diabetes. SR-BI is a membrane protein. It is originally identified as a lipoprotein receptor. Mice deficient in SR-BI have a 2-fold increase in plasma cholesterol levels and are more susceptible to atherosclerosis. Recently, my laboratory uncovered two pivotal functions of SR-BI: 1) SR-BI protects against sepsis; 2) SR-BI prevents nitric oxide-induced cytotoxicity. We currently use a combination of molecular, cellular and genetically manipulated animal models to elucidate the mechanisms underlying SR-BI to protect against sepsis and nitric oxide-induced cytotoxicity.
Project 1. Role of SR-BI in protection against sepsis.
Sepsis is one of the major causes of death that claims over 215,000 lives and costs $16.7 billion per year in America alone. The death rate remains high due to poor understanding of the disease. Using a sepsis animal model, we demonstrate that SR-BI is a critical protective factor of sepsis. The purpose of this project is to determine the mechanism whereby SR-BI protects against sepsis. This project is supported by grants from NIH and American Heart Association.
Project 2. Role of SR-BI in protection against nitric oxidative stress in atherosclerosis and diabetes.
Nitric oxide-induced oxidative stress contributes to a variety of diseases such as atherosclerosis and diabetes. We recently demonstrate that expression of SR-BI prevents nitric oxide induced cell death. Understanding the mechanism of SR-BI protection against nitric oxide induced cytotoxicity may provide more insight into the development of atherosclerosis and diabetes. This project is currently supported by grants from NIH and American Heart Association.
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