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Am J Physiol Heart Circ Physiol (January 14, 2005). doi:10.1152/ajpheart.01009.2004
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Submitted on October 4, 2004
Accepted on January 11, 2005

In Vivo Adenosine Receptor Preconditioning Reduces Myocardial Infarct Size Via Subcellular ERK Signaling

Easton A Reid1, Gentian Kristo1, Yukihiro Yoshimura1, Cherry Ballard-Croft1, Byron J Keith1, Robert M Mentzer, Jr.1, and Robert D Lasley1*

1 Department of Surgery, University of Kentucky College of Medicine, Lexington, KY, USA

* To whom correspondence should be addressed. E-mail: rlasley{at}uky.edu.

The protective effects of adenosine receptor acute preconditioning (PC) are well-known, however the signaling mechanism mediating this effect has not been determined in in vivo models. The purpose of this study was to determine the role of the extracellular signal-regulated kinase (ERK) pathway in mediating adenosine PC in in vivo rat myocardium. Open-chest rats were submitted to 25 min coronary artery occlusion and 2 hr reperfusion. ERK activation was assessed by measuring total and dually phosphorylated p44/42 ERK isoforms in nuclear/myofilament, mitochondrial, cytosolic, and membrane fractions. Adenosine receptor PC with the A1/A2a agonist AMP579 reduced infarct size from 49 ± 3% to 29 ± 3%, an effect that was blocked by the MEK inhibitor U0126. ERK isoforms were present in all fractions, with the greatest expression in the cytosolic fraction and the least in the mitochondrial fraction. AMP579 treatment increased preischemic p44/42 ERK phosphorylation in all fractions 2.7- to 6.9-fold. Reperfusion increased ERK isoform activation in all fractions, but there were no differences between control and AMP579 hearts. Preischemic increases in phospo-p44/p42 ERK with AMP579 were blunted by U0126, although only in mitochondrial and membrane compartments. The PC effects of AMP579 on infarct size and ERK were blunted by both the A1 antagonist DPCPX and, surprisingly, the A2a antagonist ZM241385. These results indicate that the unique adenosine receptor agonist AMP579 exerts its beneficial effects in vivo via both A1 and A2a receptor modulation of subcellular ERK isoform signaling.




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