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Expression and Location of Pro- and Anti-Apoptotic Proteins after Cardiac Preconditioning and Ischemia/Reperfusion
Raquel S. Carreira1,2; Lino M. Gonçalves1; Luís A. Providência1;Alicia J. Kowaltowski2
1Unidade de Investigação Básica em Cardiologia, Serviço de Cardiologia, Hospitais da Universidade de Coimbra, Coimbra, Portugal; 2Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, São Paulo, Brasil
Ischemic preconditioning protects the heart against damage promoted by ischemia/reperfusion by inhibiting both myocardial necrosis and mitochondrially-initiated apoptosis. We evaluated the expression of pro and anti-apoptotic proteins in mitochondria from hearts submitted to ischemic preconditioning. We verified that IP alone did not alter the expression or location of Bid, Bax and Bcl-2, or promote the release of cytochrome c from the mitochondria. The abundance of Bcl-xL was slightly decreased by ischemic preconditioning. Since this protein is antiapoptotic, this decrease cannot be related to loss of cell death promoted by this process. When ischemic preconditioning was followed by ischemia/reperfusion, an increase in Bcl-2 and Bcl-xL levels was observed. We conclude that IP per se does not alter the apoptotic program, but allows for changes in anti-apoptotic protein expression during ischemia/reperfusion.
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