Role of apoptosis-inducing factor in myocardial cell @entity204 by XXXX -reperfusion.

@entity66 @entity63 @entity35 @entity4124 @entity204
Although apoptosis contributes to myocardial cell @entity204 in the @entity63 -reperfused heart, the molecular basis of apoptosis is poorly understood. @entity66 ( @entity66 ) has been characterized as a caspase-independent @entity204 effector. Upon the induction of apoptosis, mitochondrial @entity66 is released to the cytoplasm and then enters the nucleus, in which it induces chromatin condensation and 50 kbp DNA fragmentation. In the present study, we examined the role of @entity66 in @entity63 -reperfusion injury in isolated @entity35 hearts. @entity66 was detected in the cytosolic and nuclear fractions of hearts subjected to @entity63 -reperfusion, whereas it was detected only in the mitochondria of control hearts. Moreover, @entity66 release increased in a reperfusion time-dependent manner. Pulse field gel electrophoresis revealed that 50 kbp DNA fragments were produced by @entity63 /reperfusion. In contrast, cytochrome c release and the activation of @entity4124 did not occur to a significant extent. Moreover, @entity63 preconditioning attenuated the @entity66 release and the 50 kbp DNA fragmentation. These results suggest that @entity66 -dependent apoptosis is likely to attribute to myocardial cell @entity204 in the @entity63 -reperfused heart and that it is related with the protective effect of @entity63 preconditioning.
