Abstract
Reperfusion of myocardial tissue can result in programmed cell death. Nevertheless, relatively little information exists concerning pathways initiated in vivo that ultimately commit cardiac cells to apoptosis during ischemia/reperfusion. The goal of the present study was to determine whether mitochondrial-mediated mechanisms of apoptosis are initiated during in vivo cardiac ischemia/reperfusion. We provide evidence that the content of cytochrome c in the cytosol increases exclusively during reperfusion. Over the same time interval Bax, a pro-apoptotic protein implicated in release of cytochrome c from mitochondria, was found to disappear from cytosolic extracts. This was associated with the appearance of tightly associated Bax in the mitochondrial fraction. Cytochrome c from reperfused cytosolic extracts is present as a high molecular weight oligomer consistent with formation of the apoptosome. In addition, pro-caspase-9 was found to disappear exclusively during reperfusion. Therefore, the results of the current study indicate that the mitochondrial-mediated pathway of apoptosis is initiated as a result of in vivo cardiac ischemia/reperfusion.
Original language | English (US) |
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Pages (from-to) | 50-57 |
Number of pages | 8 |
Journal | Archives of Biochemistry and Biophysics |
Volume | 432 |
Issue number | 1 |
DOIs | |
State | Published - Dec 1 2004 |
Keywords
- Apoptosis
- Bax
- Cytochrome c
- Heart
- Ischemia
- Mitochondria
- Reperfusion
ASJC Scopus subject areas
- Biophysics
- Biochemistry
- Molecular Biology