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Cardiomyocyte‐specific inactivation of transcription factor CREB in mice
Author(s) -
Matus Marek,
Lewin Geertje,
Stümpel Frank,
Buchwalow Igor B.,
Schneider Michael D.,
Schütz Günther,
Schmitz Wilhelm,
Müller Frank U.
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.06-7915com
Subject(s) - creb , creb1 , transcription factor , regulator , microbiology and biotechnology , biology , apoptosis , gene , genetics
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)