Xu Peng, M.D., Ph.D.
Assistant Professor
Systems Biology and Translational Medicine
702 Southwest H.K. Dodgen Loop
Temple,
TX 76504
Phone: 254-742-7176
Fax: 254-742-7145
Email: xpeng@medicine.tamhsc.edu
Education and Post-Graduate Training
M.D. (equivalent), Clinical Medicine, 1992, Shanghai Tiedao Medical College
M.S., Internal Medicine-Cardiology, 1997, Shanghai Second Medical University
Ph.D., Internal Medicine-Cardiology, 2000, Peking University
Research Interests
Cardiovascular disease is the leading cause of human mortality globally and ranks as the number one killer in the USA. Despite dramatic advances in medical treatments, there remain many unmet medical needs in the treatment of cardiovascular disease. Our long-term goal is to explore and define novel genetic mechanisms that are involved in cardiovascular disease which can ultimately translate into potential strategies for its treatment. To achieve this goal, we will use a comprehensive approach including mouse genetics and molecular and cellular biology methods to explore the mechanisms involved in the regulation of cardiovascular development and disease.
Cdc42 is a Ras-related GTPase that plays an essential role in controlling cell polarity through the regulation of the actin cytoskeletal architecture. Blocking the ability of Cdc42 to activate its effectors has been shown to inhibit a range of cellular functions including cell migration, proliferation and differentiation. Consistent with these important in vitro functions, Cdc42 gene inactivation in mice induced lethality before embryonic day 7.5. Early embryonic lethal phenotypes make it impossible to study the functions of Cdc42 in later embryonic development and in adult mice. To overcome the problem of embryonic lethality of Cdc42 total knockout mice, we have generated Cdc42/flox mice with the Cdc42 gene flanked by two loxp sites. Evidence has shown that Cdc42 plays an important role in cardiomyocyte and vascular endothelial cells, however, Cdc42 functions in cardiovascular development in vivo remain largely unknown. To explore how Cdc42 functions in vivo in the cardiovascular system, we generated several lines of vascular endothelial cell and cardiomyocyte specific Cdc42 knockout mice and will try to explore:
- How Cdc42 regulates vasculogenesis and organ-specific angiogenesis in embryonic development.
- What are the Cdc42 upstream regulators and downstream effectors in angiogenesis and vasculogenesis.
- How Cdc42 can regulate overall heart development and hypertrophy.
Selected Publications
Peng X, Wu X, Druso JE, Wei H, Park A-Y, Kraus MS, Alcaraz A, Chen J, Chien S, Cerione RA, Guan J-L. Cardiac developmental defects and spontaneous right ventricular hypertrophy in cardiomyocyte FAK conditional knockout mice. Proc Natl Acad Sciences 105:6638-6643, 2008.
Nagy T, Wei H, Shen T-L, Peng X, Liang C-C, Gan B, Guan J-L. Mammary epithelial-specific deletion of the focal adhesion kinase gene leads to severe lobulo-alveolar hypoplasia and secretory immaturity of the murine mammary gland. J Biol Chem 282:31766-31776, 2007.
Feng Q, Baird D, Peng X, Wang J, Ly T, Guan J-L, Cerione RA. The Cool-1/beta-Pix protein serves as an essential regulatory node for EGFR- and Src-mediated cell growth. Nature Cell Biol 8:945-956, 2006.
Gan B, Peng X, Nagy T, Alcaraz A, Gu H, Guan J-L. Role of FIP200 in cardiac and liver development and its regulation of TNFalpha and TSC-mTOR signaling pathways. J Cell Biol 175:121-133, 2006.
Peng X, Kraus MS, Wei H, Shen T-L, Pariaut R, Chen J, Chien K, Gu H, Guan J-L. Inactivation of FAK in cardiomyocytes promotes cardiac eccentric hypertrophy and fibrosis in mice. J Clin Invest 116:217-227, 2006.
Shen T-L, Park A Y-J, Alcaraz A, Peng X, Flavell RA, Gu H, Guan J-L. Requirement of focal adhesion kinase in both early and late embryonic development. J Cell Biol 169:941-952, 2005.
Melkoumian ZK, Peng X, Gan B, Wu X, Guan J-L. Mechanisms of cell cycle regulation by FIP200 in human breast cancerl cells. Cancer Res 65:6677-6684, 2005.
Peng X, Ueda H, Zhou H, Stokol T, Shen T-L, Alcaraz A, Nagy T, Vassalli J-D, Guan J-L. Overexpression of focal adhesion kinase in vascular enothelial cells promotes angiogenesis in transgenic mice. Cardiovasc Res 64:421-430, 2004.
