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Experimental & Molecular Medicine ; : 243-252, 2009.
Article Dans Anglais | WPRIM | ID: wpr-49343

Résumé

Oxidative stress is critical for causing cardiac injuries during ischemia-reperfusion (IR), yet the molecular mechanism for this remains unclear. In the present study, we observe that hypoxia and reoxygenation, a component of ischemia, effectively induces apoptosis in the cardiac myocytes from neonatal rats and it concomitantly leads to induction of GADD153, an apoptosis-related gene. Furthermore, IR injury of rat heart showed a GADD153 overexpression in the ischemic area where the TUNEL reaction was positive. A downregulation of cardiac ankyrin repeat protein (CARP) was also observed in this ischemic area. Promoter deletion and reporter analysis revealed that hypoxia transcriptionally activates a GADD153 promoter through the AP-1 element in neonatal cardiomyocytes. Ectopic overexpression of GADD153 resulted in the downregulation of CARP expression. Accordingly, the induction of GADD153 mRNA were followed by the CARP down-regulation in an in vivo rat coronary ischemia/reperfusion injury model. These results suggest that GADD153 over-expression and the resulting downregulation of CARP may have causative roles in apoptotic cell death during cardiac IR injury.


Sujets)
Animaux , Humains , Mâle , Rats , Animaux nouveau-nés , Hypoxie , Apoptose/physiologie , Cellules cultivées , Lésion de reperfusion myocardique/métabolisme , Myocarde/métabolisme , Myocytes cardiaques/cytologie , Protéines nucléaires/génétique , Régions promotrices (génétique) , Rat Sprague-Dawley , Protéines de répression/génétique , Facteur de transcription AP-1/génétique , Facteur de transcription CHOP/génétique
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