Circulation Research. 2002;90:745-748
Published online before print March 14, 2002, doi: 10.1161/01.RES.0000015224.07870.9A
Published online before print March 14, 2002, doi: 10.1161/01.RES.0000015224.07870.9A
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© 2002 American Heart Association, Inc.
Molecular Medicine |
Different Signaling Pathways Induce Apoptosis in Endothelial Cells and Cardiac Myocytes During Ischemia/Reperfusion Injury
From the Medical Molecular Biology Unit (T.M.S., A.S., D.S.L.), Institute of Child Health, University College London, UK; the Cardiovascular Pathophysiology Research Centre (E.P., L.C.), University of Ferrara, Italy; the Chair of Cardiology (R.R), University of Brescia, Italy; and the National Heart and Lung Institute (R.A.K.), Royal Brompton Hospital, London, UK.
Correspondence to Tiziano M. Scarabelli, Medical Molecular Biology Unit, Institute of Child Health, University College London, 30 Guilford St, London WC1N 1EH, UK. E-mail tscarabelli{at}hotmail.com
Apoptosis contributes, with necrosis, to the cardiac cell loss after ischemia/reperfusion injury. The apoptotic cascade is initiated either by mitochondrial damage and activation of caspase-9 or by death receptor ligation and activation of caspase-8. In the present study, performed in the isolated rat heart exposed either to ischemia alone or ischemia followed by reperfusion, cleavage of caspase-9 was observed primarily in endothelial cells. Conversely, caspase-8 cleavage was only found in cardiomyocytes, where it progressively increased throughout reperfusion. Addition of a specific caspase-9 inhibitor to the perfusate before ischemia prevented endothelial apoptosis, whereas preischemic infusion of a specific caspase-8 inhibitor affected only myocyte apoptosis. Additionally, caspase-8–mediated BID processing was observed only during reperfusion. Production of tBID then sustains mitochondrial injury and perpetuates caspase-9 activation.
Key Words: apoptosis • endothelium • myocytes • ischemia • reperfusion
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