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Am J Physiol Heart Circ Physiol 284: H859-H866, 2003; doi:10.1152/ajpheart.00251.2002
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Vol. 284, Issue 3, H859-H866, March 2003

A1 adenosine receptor overexpression attenuates ischemia-reperfusion-induced apoptosis and caspase 3 activity

Sara E. Regan1,4, Michael Broad2, Anne M. Byford1,4, Amy R. Lankford1,4, Rachael J. Cerniway1, Marty W. Mayo3, and G. Paul Matherne1,4

Departments of 1 Pediatrics, 2 Surgery, and 3 Biochemistry and Molecular Genetics, and the 4 Cardiovascular Research Center, University of Virginia Health System, Charlottesville, Virginia 22908

We tested the hypothesis that myocardial ischemia-reperfusion (I/R)-induced apoptosis is attenuated in transgenic mice overexpressing cardiac A1 adenosine receptors. Isolated hearts from transgenic (TG, n = 19) and wild-type (WT, n = 22) mice underwent 30 min of ischemia and 2 h of reperfusion, with evaluation of apoptosis, caspase 3 activity, function, and necrosis. I/R-induced apoptosis was attenuated in TG hearts. TG hearts had less I/R-induced apoptotic nuclei (0.88 ± 0.10% vs. 4.22 ± 0.24% terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive cells in WT, P < 0.05), less DNA fragmentation (3.30 ± 0.38-fold vs. 4.90 ± 0.39-fold over control in WT, P < 0.05), and less I/R-induced caspase 3 activity (145 ± 25% over nonischemic control vs. 234 ± 31% in WT, P < 0.05). TG hearts also had improved recovery of function and less necrosis than WT hearts. In TG hearts pretreated with LY-294002 (3 µM) to evaluate the role of phosphosinositol-3-kinase in acute signaling, there was no change in the functional protection or apoptotic response to I/R. These data suggest that cardioprotection with transgenic overexpression of A1 adenosine receptors involves attenuation of I/R-induced apoptosis that does not involve acute signaling through phosphoinositol-3-kinase.

cardioprotection; ischemia-reperfusion injury; transgenic mice; phosphoinositol-3-kinase


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