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Published online before print February 16, 2007 as doi: 10.1096/fj.06-7915com.

Cardiomyocyte-specific inactivation of transcription factor CREB in mice

Marek Matus, Geertje Lewin, Frank Stümpel, Igor B. Buchwalow, Michael D. Schneider, Günther Schütz, Wilhelm Schmitz, and Frank U. Müller

E-mail contact: mullerf@uni-muenster.de

The transcription factor cAMP response element (CRE)-binding protein (CREB, Creb1) plays a critical role in regulating gene expression in response to activation of the cAMP-dependent signaling pathway, which is implicated in the pathophysiology of heart failure. Using the Cre-loxP system, we generated mice with a cardiomyocyte-specific inactivation of CREB and studied in this model whether CREB is critical for cardiac function. CREB-deficient mice were viable and displayed neither changes in cardiac morphology nor alterations of basal or isoproterenol-stimulated left ventricular function in vivo or of important cardiac regulatory proteins. Since CREB was proposed as a negative regulator of cardiomyocyte apoptosis by enhancing the expression of the antiapoptotic protein Bcl-2, we analyzed the fragmentation of DNA, the activity of caspases 3/7 and the expression of Bcl-2 and did not observe any differences between CREB-deficient and CREB-normal hearts. Our results suggest that the presence of CREB is not critical for normal cardiac function in mice.--Matus M., Lewin G., Stümpel F., Buchwalow I. B., Schneider M. D., Schütz G., Schmitz W., and Müller F. U. Cardiomyocyte-specific inactivation of transcription factor CREB in mice.




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