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Division of Cardiology, Department of Medicine, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia 23298
We investigated the role of p38 mitogen-activated protein kinase (MAPK) phosphorylation and opening of the mitochondrial ATP-sensitive K+ [(KATP)mito] channel in the adenosine A1 receptor (A1AR)-induced delayed cardioprotective effect in the mouse heart. Adult male mice were treated with vehicle (5% DMSO) or the A1AR agonist 2-chloro-N6-cyclopentyladenosine (CCPA; 0.1 mg/kg ip). Twenty-four hours later, hearts were subjected to 30 min of global ischemia and 30 min of reperfusion in the Langendorff mode. Genistein or SB-203580 (1 mg/kg ip) given 30 min before CCPA treatment was used to block receptor tyrosine kinase or p38 MAPK phosphorylation, respectively. 5-Hydroxydecanoate (5-HD; 200 µM) was used to block (KATP)mito channels. CCPA produced marked improvement in left ventricular function, which was partially blocked by SB-203580 and 5-HD and completely abolished with genistein. CCPA caused a reduction in infarct size (12.0 ± 2.0 vs. 30.3 ± 3.0% in vehicle), which was blocked by genistein (29.4 ± 2.3%), SB-203580 (28.3 ± 2.6%), and 5-HD (33.9 ± 2.4%). CCPA treatment also caused increased phosphorylation of p38 MAPK during ischemia, which was blocked by genistein, SB-203580, and 5-HD. The results suggest that A1AR-triggered delayed cardioprotection is mediated by p38 MAPK phosphorylation. Blockade of cardioprotection with 5-HD concomitant with decrease in p38 MAPK phosphorylation suggests a potential role of (KATP)mito channel opening in phosphorylation and ensuing the late preconditioning effect of A1AR.
ischemia; reperfusion myocardial infarction; adenosine; ATP-sensivitive potassium channel; signaling transduction; mitogen-activated protein
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