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Abstract
Platelets protect myocardium against ischemia-reperfusion injury. This study examined the role of platelet-derived TGF-β1 in cardioprotection during ischemia-reperfusion. Isolated Sprague Dawley rat hearts were perfused with K-H buffer and subjected to 25 min of global ischemia followed by 30 min of reperfusion. Ischemia-reperfusion resulted in myocardial dysfunction indicated by increase in CPP and LVEDP, and decrease in dLVP. Perfusion of hearts with washed platelets or supernatant of aggregated platelets attenuated (P < 0.01) of myocardial dysfunction following ischemia-reperfusion. Ischemia-reperfusion resulted in a decrease in myocardial TGF-β1 determined by immunohistochemistry. ELISA showed an increase in latent TGF-/β1, but a decrease in active TGF-β1, Perfusion of hearts with platelets or aggregated platelet supernatant preserved myocardial TGF-β1 content upon ischemia-reperfusion. Perfusion of hearts with recombinant TGF-β1 also resulted in cardioprotection following ischemia-reperfusion qualitatively similar to that observed with platelets or aggregated platelet supernatants. RT-PCR analysis showed an increase in myocardial TGF-β1 mRNA following ischemia-reperfusion. These observations indicate that platelets protect the myocardium against ischemia-reperfusion-mediated dysfunction at least in part by releasing TGF-β1. Increase in both TGF-β1 mRNA and latent TGF-β1 does not indicate a defect in the translation of mRNA. Reduction in myocardial TGF-β1 following ischemia-reperfusion suggests a defect in the conversion of latent TGF-β1 to active TGF-β1.