Key result
Cardiomyocyte-specific inactivation of CREB in mice did not alter cardiac morphology, left ventricular function, or apoptosis markers compared to CREB-normal hearts.
Why the study?
Does cardiomyocyte-specific inactivation of CREB alter cardiac function or apoptosis in mice?
Does cardiomyocyte-specific inactivation of CREB alter cardiac function or apoptosis in mice?
Cardiomyocyte-specific inactivation of CREB is not critical for normal cardiac function or apoptosis regulation in mice.
CREB inactivation does not affect basal murine cardiac function; leaves open its role under stress or in human disease.
The transcription factor cAMP response element (CRE)‐binding protein (CREB, Crebl) 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., Stumpel F., Buchwalow I. B., Schneider M. D., Schlitz G., Schmitz W., and Müller F. U. Cardiomyocyte‐specific inactivation of transcription factor CREB in mice. FASEB J. 21, 1884–1892 (2007)
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Máťuš et al. (2007) studied Cardiac function. Cardiomyocyte-specific inactivation of CREB vs. CREB-normal hearts was evaluated on Cardiac morphology, left ventricular function, and apoptosis markers. Cardiomyocyte-specific inactivation of CREB in mice did not alter cardiac morphology, left ventricular function, or apoptosis markers compared to CREB-normal hearts.
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