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Papers In Press, published online ahead of print September 19, 2005
Department of Surgery, Columbia University, New York, NY 10032
Corresponding Author: gx15{at}columbia.edu
Vitamin D3 upregulated protein 1(VDUP1) is a key mediator of oxidative stress on various cellular processes via downstream effects on apoptosis signaling kinase 1 (ASK1) and p38 mitogen-activated protein kinase (MAPK). Here, we report that VDUP1 expression is significantly increased in rat hearts following acute myocardial ischemia, suggesting it may have important regulatory effects on cardiac physiological processes during periods of oxidative stress. Transfection of H9C2 cardiomyoblasts with a sequence-specific VDUP1 DNA enzyme to downregulate VDUP1 mRNA expression significantly reduced apoptosis and enhanced cell survival under conditions of H2O2 stress, and these effects involved inhibition of ASK1 activity. Direct intracardiac injection of the DNA enzyme at the time of acute myocardial infarction reduced myocardial VDUP1 mRNA expression, and resulted in prolonged reduction in cardiomyocyte apoptosis. Moreover, downregulation of VDUP1 was accompanied by significant reduction in cardiac expression of procollagen type I alpha2 mRNA level, as well as marked reduction in myocardial scar formation. These features were accompanied by significant improvement in cardiac function. Together, these results suggest a direct role for VDUP1 in the adverse effects of ischemia and oxidative stress on cardiomyocyte survival, left ventricular collagen deposition, and cardiac function. Strategies to inhibit VDUP1 expression and/or function during acute ischemic events may be beneficial to cardiac functional recovery and prevention of left ventricular remodeling.
J. Biol. Chem, 10.1074/jbc.M502966200
Submitted on March 17, 2005
Revised on September 8, 2005
Accepted on September 18, 2005
Catalytic degradation of vitamin D3 upregulated protein1 (VDUP1) mRNA enhances cardiomyocyte survival and prevents left ventricular remodeling after myocardial ischemia
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