作者: Tinggui Yin , Gulzar Sandhu , Curt D Wolfgang , Althea Burrier , Randy L Webb
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摘要: In this report we investigate the molecular mechanisms that contribute to tissue damage following ischemia and coupled with reperfusion (ischemia/reperfusion) in rat heart kidney. We observe activation of three stress-inducible mitogen-activated protein (MAP) kinases these tissues: p38 MAP kinase 46- 55-kDa isoforms Jun N-terminal (JNK46 JNK55). The kidney show distinct time courses during but no either JNK46 or JNK55. These two tissues also respond differently ischemia/reperfusion. JNK55 kinase, whereas all are active. examined expression pattern stress-responsive genes, c-Jun ATF3. Our results indicate both genes induced by However, ATF3 is only To correlate events DNA laddering, a common marker apoptosis. A significant increase laddering was evident ischemia/reperfusion correlated activation, supporting link between stress apoptotic cell death tissues.