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Different signaling pathways induce apoptosis in endothelial cells and cardiac myocytes during ischemia/reperfusion injury.

Authors: Scarabelli, Tiziano M  Stephanou, Anastasis  Pasini, Evasio  Comini, Laura  Raddino, Riccardo  Knight, Richard A  Latchman, David S 
Citation: Scarabelli TM, etal., Circ Res. 2002 Apr 5;90(6):745-8.
Pubmed: (View Article at PubMed) PMID:11934844

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.


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RGD Object Information
RGD ID: 13782263
Created: 2018-08-30
Species: All species
Last Modified: 2018-08-30
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.