Chuanxi Cai, PhD
Assistant Professor of Medicine
Email Dr. Cai
Ph.D.: 1998-2004, Institute of Biophysics in Chinese Academy of Sciences
Postdoctoral Fellow: 2004-2009, Physiology and Biophysics in UMDNJ
AHA Postdoctoral Fellowship: 2008-2009, Physiology and Biophysics in UMDNJ
Assistant Professor: 2009-present, University of Louisville School of Medicine
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 during acute myocardial infarction, and to develop cellular or genetic therapeutic approaches for preventing myocardial injury, promoting the regeneration following cardiac muscle damage, and treatment for patients with ischemic heart disease. Specifically, the current projects in my laboratory include the use of adult stem/progenitor cells, and inducible pluripotent stem cells for myocardial repair on the therapeutic applications of cell-based therapies in cardiovascular diseases. 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.
- 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 Extracellular Signal-regulated Kinase (ERK)/NRF2 Signaling Pathway and Cytokine Release. J Biol Chem. 2012 Sep 28;287(40):33720-32. Epub 2012 Aug 9.
- Lin P, Zhu H, Cai C, Wang X, Cao C, Xiao R, Pan Z, Weisleder N, Takeshima H, Ma J. Nonmuscle myosin IIA facilitates vesicle trafficking for MG53-mediated cell membrane repair. FASEB J. 2012 May;26(5):1875-83. Epub 2012 Jan 17.
- Cai C, Weisleder N, Ko JK, Komazaki S, Sunada Y, Nishi M, Takeshima H, 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. Epub 2009 Apr 20.
- Li N, Lin P, Cai C, Pan Z, Weisleder N, Ma J. The amino-terminal peptide of Bax perturbs intracellular Ca2+ homeostasis to enhance apoptosis in prostate cancer cells. Am J Physiol Cell Physiol. 2009 Feb;296(2):C267-72. Epub 2008 Dec 17.
- Cai C, Masumiya H, Weisleder N, Matsuda N, Nishi M, Hwang M, Ko JK, Lin P, Thornton A, Zhao X, Pan Z, Komazaki S, Brotto M, Takeshima H, Ma J. MG53 nucleates assembly of cell membrane repair machinery. Nat Cell Biol. 2009 Jan;11(1):56-64. Epub 2008 Nov 30.
- 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. Epub 2008 Nov 24.
- Cai C, Lin P, Cheung KH, Li N, Levchook C, Pan Z, Ferrante C, Boulianne GL, Foskett JK, 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. Epub 2006 Apr 7.
- 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, 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.