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Transcription factor AP-2alpha triggers apoptosis in cardiac myocytes.

Authors: Muller, FU  Loser, K  Kleideiter, U  Neumann, J  Von Wallbrunn, C  Dobner, T  Scheld, HH  Bantel, H  Engels, IH  Schulze-Osthoff, K  Schmitz, W 
Citation: Muller FU, etal., Cell Death Differ. 2004 May;11(5):485-93.
Pubmed: (View Article at PubMed) PMID:14752511
DOI: Full-text: DOI:10.1038/sj.cdd.4401383

Idiopathic-dilated cardiomyopathy (IDC) is a common primary myocardial disease of unknown etiology associated with apoptosis, cardiac dilatation, progressive heart failure and increased mortality. An elevation of the transcription factor activator protein 2alpha (AP-2alpha) is involved in vertebrate embryonic development and oncogenesis. Here, we show that AP-2alpha protein is expressed in the human heart and increased in human failing myocardium with IDC. Adenovirus-mediated overexpression of human AP-2alpha triggered apoptosis and increased mRNA levels of Bcl-2 family members Bax and Bcl-x in rat cardiomyocytes. Immunohistological analysis of human myocardium revealed an increased percentage of AP-2alpha-positive nuclei in IDC and, interestingly, a colocalization of AP-2alpha-positive but not -negative cells with a caspase-cleaved fragment of poly(ADP-ribose)polymerase. We suggest AP-2alpha as a novel cardiac regulator implicated in the activation of apoptosis in IDC.

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CRRD Object Information
CRRD ID: 1578494
Created: 2006-03-24
Species: All species
Last Modified: 2006-03-24
Status: ACTIVE



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