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Am J Physiol Heart Circ Physiol (December 11, 2003). doi:10.1152/ajpheart.00953.2003
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Submitted on October 9, 2003
Accepted on November 24, 2003

Differential regulation of activator protein-1 and heat shock factor-1 in myocardial ischemia and reperfusion injury: role of poly(ADP-ribose) polymerase-1

Basilia Zingarelli1*, Paul W. Hake1, Michael O'Connor1, Alvin Denenberg1, Hector R. Wong1, Sue Kong1, and Bruce J. Aronow1

1 Critical Care Medicine, Cincinnati Children's Hospital, Cincinnati, OHIO, USA

* To whom correspondence should be addressed. E-mail: basilia.zingarelli{at}cchmc.org.

Poly(ADP-ribose) polymerase-1 (PARP-1), a nuclear enzyme activated in response to DNA strand breaks, has been implicated in cell dysfunction in myocardial reperfusion injury. PARP-1 has also been shown to participate in transcription and regulation of gene expression. In this study we investigated the role of PARP-1 on the signal transduction pathway of activator protein-1 (AP-1) and heat shock factor-1 (HSF-1) in myocardial reperfusion injury. Mice genetically deficient of PARP-1 (PARP-1-/-) exhibited a significant reduction of myocardial damage after occlusion and reperfusion of the left anterior descending branch of the coronary artery when compared to their wild-type littermates. This cardioprotection was associated with reduction of the phosphorylative activity of c-Jun NH2 terminal kinase (JNK) and, subsequently, reduction of the DNA binding of the signal transduction factor AP-1. On the contrary, in PARP-1-/- mice DNA binding of HSF-1 was enhanced and was associated with a significant increase of the cardioprotective heat shock protein (HSP) 70 when compared to wild-type mice. Microarray analysis revealed that expression of several AP-1-dependent genes of proinflammatory mediators and HSPs was altered in PARP-1-/- mice. The data indicate that PARP-1 may exert a pathological role in reperfusion injury by functioning as an enhancing factor of AP-1 activation and as a repressing factor of HSF-1 activation and HSP70 expression.




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