Associate Professor of Cardiovascular Medicine
Institute of Biophysics, Beijing, P.R. China
Wuhan University, P.R. China
Ischemic heart disease remains as the single largest cause of mortality in western countries. A major challenge in the field of molecular cardiology is developing novel therapeutic approaches to prevent injury and to facilitate recovery of cells that are constantly undergoing physiological stress. My long term research interests are to understand the molecular and cellular mechanism for myocardial repair and regeneration after myocardial infarction, and to develop molecular and cellular therapeutic approaches for preventing myocardial injury, promoting the regeneration following cardiac muscle damage, and treatment for patients with heart diseases. Specifically, the current projects in my laboratory include the use of preconditioned adult stem/progenitor cells for myocardial repair on the therapeutic applications for cardiovascular diseases, as well as understanding the role of muscle specific TRIM family protein, MG53, in healthy and diseased heart. To achieve our goals, we will use multidisciplinary approaches that include biochemistry, molecular biology, cell biology, and genetic analysis through the modulation of mouse models.
1. Enhancing the effectiveness of human cardiac stem cell therapy; 2. The role of MG53 (TRIM72) in cardiac development and regeneration;
- Cai, C., Chen, J. Overexpression of caveolin-1 induces alteration of multidrug resistance in Hs578T breast adenocarcinoma cells. Int J Cancer. 2004 Sep 10; 111(4):522-9.
- Cai, C., Zhu, H., Chen, J. Overexpression of caveolin-1 increases plasma membrane fluidity and reduces P-glycoprotein function in Hs578T/Dox. Biochem Biophys Res Commun. 2004 Jul 30; 320(3):868-74.
- Cai, C., Lin, P., Cheung, KH., Li, N., Levchook, C., Pan, Z., Ferrante, C., Boulianne, GL., Foskett, J.K., Danielpour, D., Ma, J. The presenilin-2 loop peptide perturbs intracellular Ca2+ homeostasis and accelerates apoptosis. J Biol Chem. 2006 Jun 16; 281(24):16649-55.
- Cai, C., Masumiya, H., Weisleder, N., Pan, Z., Nishi, M., Komazaki, S., Takeshima, H., Ma, J. MG53 regulates membrane budding and exocytosis in muscle cells. J Biol Chem. 2009 Jan 30; 284(5):3314-22.
- Cai, C., Masumiya, H., Weisleder, Matsuda, N., Nishi, M., Hwang, M., Ko, J., Lin, P., Thornton, A., Zhao, X., Pan, Z., Brotto, M., Komazaki, S., Takeshima, H. and Ma, J. MG53 nucleates assembly of membrane repair machinery. Nat Cell Biol. 2009 Jan; 11(1):56-64.
- Cai, C., Weisleder, N., Ko, J., Komazaki, S., Sunada, Y., Nishi, M., Takeshima, H. and Ma, J. Membrane repair defects in muscular dystrophy are linked to altered interaction between MG53, caveolin-3 and dysferlin. J Biol Chem. 2009 Jun 5; 284(23):15894-902.
- Weisleder N, Takizawa N, Lin P, Wang X, Cao C, Zhang Y, Tan T, Ferrante C, Zhu H, Chen PJ, Yan R, Sterling M, Zhao X, Hwang M, Takeshima M, Cai, C., Cheng H, Takeshima H, Xiao RP, Ma J. Recombinant MG53 protein modulates therapeutic cell membrane repair in treatment of muscular dystrophy. Sci Transl Med. 2012 Jun 20; 4(139):139ra85.
- Cai, C., Teng, L,, Vu, D., He, JQ., Guo, Y., Li, Q., Tang, XL., Rokosh, G., Bhatnagar, A., Bolli, R. The Heme Oxygenase 1 Inducer (CoPP) Protects Human Cardiac Stem Cells Against Apoptosis Through Activation of The ERK/Nrf2 Signaling Pathway and Cytokine Release. J Biol Chem. 2012 Sep 28; 287(40):33720-32.
- CaiLab Web Site
- NIH Grants