Mengwei Zang
Assistant Professor
Education:
1998 Ph.D., Pharmacology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, P.R.China
1998-1999 Postdoctoral Fellow, Cell Biology and Pharmacology, The Center for Basic Research in Digestive Diseases, Mayo Clinic and Foundation, Rochester, MN
1999-2003 Postdoctoral Fellow, Molecular Biology and Signal Transduction, Diabetes and Metabolism Unit, Boston University School of Medicine, MA
General field of research:
Cell metabolism and Diabetes
Affiliations other than medicine:
Evans Center for Interdisciplinary Biomedical Research
Vascular Biology Unit, Department of Medicine
Contact information:
Office
650 Albany Street, X726
Phone: (617)-638 2799
Lab
Phone: (617)-638 2796
Fax: (617)-638 7113
Other research websites:
Research group information
Dr. Hongliang Li, Postdoc Fellow
Phone: 617-638-2796
Email: honglli@bu.edu
Dr. Leon Li, Postdoc Fellow
Phone: 617-638-2796
Email: leonli@bu.edu
Dr. Huanxing Sun, Postdoc Fellow
Phone: 617-638-2796
Email: Huanxing@bu.edu
Frank Huo, MD Graduate Student
Phone: 617-638-2796
Email: fhao@bu.edu
Keywords:
Diabetes; Atherosclerosis; Protein kinase; NAD-dependent deacetylase; Cell Metabolism; Hepatocyte
Summary of research interest:
The main goal of Dr. Zang’s laboratory is to investigate the physiological and pathological regulation of novel nutrient signaling in energy homeostasis and in diabetes and its cardiovascular complications. A major focus is to determine how protein kinases or their signaling networks modulate hepatic glucose and lipid metabolism through regulation of kinase phosphorylation, protein-protein interactions and gene expression, and their implication in the pathogenesis of diabetes. Recent studies have focused on the role of key nutrient sensors, such as AMP-activated protein kinase (AMPK) and the NAD-dependent deacetylase (SIRT1), in the control of cell metabolism and diabetes, and found that AMPK is required for metformin, an anti-diabetic drug, to prevent hepatocyte lipid accumulation. Importantly, she has identified AMPK activation as a novel molecular mechanism for the beneficial effects of nature products, such as polyphenols including resveratrol, on hepatic lipid accumulation, hyperlipidemia and atherogenesis in diabetic mice. She and her colleagues have also defined SIRT1 as a critical regulator responsible for activation of LKB1/AMPK signaling by polyphenols, which explains their therapeutic effects on hepatocyte lipid accumulation, obesity and insulin resistance. The ultimate goal is to provide new insight into the mechanism of dyslipidemia and diabetes and identification of potential therapeutic interventions.
Recent publications:
Hou X, Xu S, Maitland-Toolan KA, Sato K, Jiang B, Ido Y, Lan F, K. Walsh, Wierzbicki M, Verbeuren TJ, Cohen RA, Zang M. 2008. SIRT1 regulates hepatocyte lipid metabolism through activating AMP-Activated protein kinase. Journal of Biological Chemistry; 283: 20015-26.
Zang M, Gong J, Luo L, Zhou J, Xiang X, Huang W, Huang Q, Luo X, Olbrot M, Peng Y, Chen C, Luo Z. 2008. Characterization of S338 phosphorylation for Raf-1 activation. Journal of Biological Chemistry; 283: 31429-37.
Zang M, Xu S, Maitland-Toolan KA, Zuccollo A, Hou X, Jiang B, Wierzbicki M, Verbeuren TJ, Cohen RA. 2006. Polyphenols stimulate AMP-activated protein Kinase, lower lipids, and inhibit accelerated atherogenesis in diabetic LDL receptor-deficient mice. Diabetes; 55: 2180-2191.
Zuccollo A, Shi C, Mastroianni R, Maitland KA, Weisbrod RM, Zang M, Xu S, Cayatte A, Corda S, Lavielle G, Verbeuren TJ, Cohen RA. 2005. The thromboxane A2 receptor antagonist, S18886, prevents enhanced atherogenesis caused by diabetes mellitus. Circulation; 112: 3001-3008.
Zang M, Zuccollo A, Hou X, Nagata D, Walsh K, Herscovitz H, Brecher P, Ruderman NB, Cohen RA. 2004. AMP-activated protein kinase is required for the lipid-lowering effect of metformin in insulin-resistant human HepG2 cells. Journal of Biological Chemistry; 279:47898-47905.
Zang M, Dong M, Pinon DI, Ding X, Hadac EM, Miller LJ. 2003. Spatial approximation between a photolabile residue in position 13 of secretin and the amino-terminal tail of the secretin receptor. Molecular Pharmacology; 63: 993-1001.
Zang M, Hayne C, Luo Z. 2002. Interaction between active Pak1 and Raf-1 is necessary for phosphorylation and activation of Raf-1. Journal of Biological Chemistry; 277: 4395-4405.
Technologies available for sharing upon request:
Molecular Biology; Protein Biochemistry; Protein kinase Assay; Protein-protein interaction; Diabetes mouse model; Atherosclerotic mouse model.
