Huiping Zhou, Ph.D.
Assistant Professor

Phone: (804) 828-6817
Dept. Fax: (804) 828-9946
e-mail: hzhou@vcu.edu

Address:
Department of Microbiology & Immunology
Virginia Commonwealth University
P.O. Box 980678
1217 East Marshall Street, 533 Medical Sciences Building
Richmond, VA 23298-0678

Professional Experience

• B.S., 1986, China Pharmaceutical University , Nanjing , Jiangsu , P.R.China
• M.S., 1989, China Pharmaceutical University , Nanjing , Jiangsu , P.R.China
• Ph.D., 1998, College of Pharmacy , University of Kentucky
• Postdoctoral, 1998-1999, College of Pharmacy , University of Kentucky
• Senior research scientist, 1999-2004, Medical College of Virginia/Virginia Commonwealth University

Research Interests:

The acquired human immunodeficiency syndrome (AIDS) epidemic has rapidly expanded since the discovery of the human immunodeficiency virus (HIV) as the cause of this disease in 1983.  By the end of November, 2007, the estimated number of people living with HIV reached 33.2 million world-wide.  More than 25 million people have died of AIDS since 1981.  HIV protease inhibitors (PIs) have been used successfully in highly active anti-retroviral therapy (HAART) for HIV infection, which is the most effective treatment currently available.  Incorporation of HIV PIs in HAART causes profound and sustained suppression of viral replication, significantly reduces the morbidity and mortality, and prolongs the lifespan of patients with HIV infection.  Unfortunately, these drugs are very toxic and the benefits of HAART are compromised by serious side effects.  One of the most deleterious side effects of HIV PI therapy is the development of dyslipidemia, which is a well established risk factor for the development of atherosclerosis.  Numerous clinic observations have suggested that HIV PIs are closely linked to atherosclerotic cardiovascular disease, which is becoming an important cause of morbidity and mortality in HIV infected patients. Association of HIV PIs with substantial metabolic abnormalities leading to atherosclerosis and hepatic lipotoxicity is a major concern for long-term use of HIV PIs in treatment of HIV infection.  Although the mechanism underlying HIV PI-induced atherosclerosis and hepatotoxicity remains to be fully identified, an increasing body of evidence suggests that multiple mechanisms may be involved, and individual PIs may have different effects on lipid metabolism. 

My laboratory has four main areas of interest. First, to identify the molecular and cellular mechanism by which HIV PIs induce dyslipidemia and atherosclerosis. Second, to understand the signaling processes and molecular mechanisms by which HIV PIs induce the inflammatory responses. Third, to determine the underlying mechanism of HIV PI-induced hepatotoxicity.  Fourth, an increasing amount of attention has been paid to use of complementary and alternative medicine (CAM) as a part of the treatment for HIV infection and the complications associated with HAART. Another ongoing project is screening potential Chinese medicines which can counteract some of the side effects caused by current HIV PIs.

Selected Publications:

Zhou H and Tai HH.  Characterization of recombinant human CXCR4 in insect cells.  Role of extracellular domains and N-glycosylation in ligand binding.  Arch. Biochem Biophys 369(2): 267-276, 1999.

Zhou H and Tai HH  Site-directed mutagenesis of human CXCR4 in insect cells.  Role of cysteinyl and negatively charged residues in ligand binding.  Arch Biochem Biophys  373 (1): 211-217, 2000.

Zhou H, Yan F and Tai HH.  Phosphorylation and desensitization of the human thoromboxane receptor alpha by G protein coupled receptor kinases.  J Pharmacol Exp Ther 298: 1243-1251, 2001.

Zhou H and Murthy KS.  Identification of the G protein-activating sequence of the single-transmembranne natriuretic peptide clearance receptor (NPR-C).  Am J Physiol Cell Physiol 284: C1255-61, 2003.

Zhou H, Sankar D, and Murthy KS.  ERK1/2-and p38 MAP kinase-dependent phosphorylation and activation of cPLA2 by m3 and m2 receptors.  Am J Physiol Gastrointest Liver Physiol 284:G472-80, 2003.

Zhou H and Murthy KS.  Distinctive G protein-dependent signaling in smooth muscle by sphingosine-1-phosphate receptors S1P₁ and S1P₂.  Am J Physiol Cell Physiol. 286(5):C1130-8, 2004

Zhou H, Pandak WM, Lyall V, Natarajan R and Hylemon PB.  HIV Protease Inhibitors Activate the Unfolded Protein Response in Macrophages: Implication for Atherosclerosis and Cardiovascular Disease.  Mol. Pharmacol. 68:690-700, 2005 

Zhou H, Huang J and Murthy KS.  Molecular cloning and functionally expression of a VIP-specific receptor.  Am J Physiol Gastrointest Liver Physiol. 291(4):G728-34, 2006.

Zhou H, Pandak WM, Jr., and Hylemon PB.  Cellular mechanisms of lipodystrophy induction by HIV protease inhibitors. Future Lipidol. 1(2): 163-172, 2006.

Zhou H, Gurley, E, Jarujaron S, Ding, Hong, Pandak,WM. Jr., Hylemon, PB. HIV protease inhibitors activate the unfolded protein response and disrupt lipid metabolism in primary hepatocytes. Am J Physiol Gastrointest Liver Physiol. 291(6):G1071-80, 2006.

Zhou H, Jarujaron S, Gurley EC, Chen L, Ding, Hong, Studer E, Hu W, Pandak,WM. Jr., Zou T, Wang JY and Hylemon, PB. HIV protease inhibitors increase TNF-α and IL-6 expression in macrophages: Involvement of the RNA binding protein HuR.  Atherosclerosis 195(1): e134-143, 2007.

Liang G, Li XK, Chen L, Yang S, Wu X, Studer E, Gurley, E, Hylemon, PB, Ye, FQ,  Li, YR and Zhou, H.  Synthesis and anti-inflammatory activities of mono-carbonyl analogues of curcumin.  Bioorg. Med. Chem. Lett.  18:1525-1529, 2008

Wu X, Zhang L, Shang J, Wang T, Wang C, Gurley E, Studer E, Yan M, Jiang Z,  Hylemon PB, Sanyal AJ, Pandak WM, and Zhou H.  Prevention of free fatty acid-  induced hepatic lipotoxicity by 18β-glycyrrhetinic acid: through both  lysosomal and mitochondrial pathways.  Hepatology  47 (6):1905-15, 2008.

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