Xiang-An Li, Ph.D. Assistant Professor Department of Pediatrics 
B365
BBSRB Department
of Pediatrics Academic Appointments: •
Department of Pediatrics, College of Medicine
Education: Awards: Sasakawa Medical Scholarship
Specific Interest in Nutrition:
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.
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.
Representative publications:
Li XA,
Guo L, Dressman J, Asmis R, Smart EJ.
A novel ligand-independent
apoptotic pathway induced by scavenger receptor class B, type I
and suppressed by endothelial nitric-oxide synthase and high
density lipoprotein. J Biol Chem. 2005, 280:19087-96.
Li XA,
Guo L, Asmis R, Nikolova-Karakashian M, Smart EJ. Scavenger
receptor BI Prevents Nitric Oxide-induced Cytotoxicity and
Endotoxin-induced Death. Circ. Res. 2006, 98: 60-65.
Babamusta F,
Rateri DL, Moorleghen JJ,
Howatt DA,
Li XA,
Daugherty A.
Angiotensin II infusion induces
site-specific intra-laminar hemorrhage in macrophage
colony-stimulating factor-deficient mice. Atherosclerosis 2006,
186: 282-290.
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