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Biochem Biophys Res Commun. 2014 Feb 28;445(1):244-9. doi: 10.1016/j.bbrc.2014.01.186. Epub 2014 Feb 6.

Annexin A7 deficiency potentiates cardiac NFAT activity promoting hypertrophic signaling.

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Department of Physiology, University of Tübingen, Tübingen, Germany.
Department of Cardiology and Cardiovascular Medicine, University of Tübingen, Tübingen, Germany.
Center for Biochemistry, Institute of Biochemistry I, University of Cologne, Köln, Germany.
Department of Physiology, University of Tübingen, Tübingen, Germany. Electronic address:


Annexin A7 (Anxa7) is a cytoskeletal protein interacting with Ca(2+) signaling which in turn is a crucial factor for cardiac remodeling following cardiac injury. The present study explored whether Anxa7 participates in the regulation of cardiac stress signaling. To this end, mice lacking functional Anxa7 (anxa7(-/-)) and wild-type mice (anxa7(+/+)) were investigated following pressure overload by transverse aortic constriction (TAC). In addition, HL-1 cardiomyocytes were silenced with Anxa7 siRNA and treated with isoproterenol. Transcript levels were determined by quantitative RT-PCR, transcriptional activity by luciferase reporter assay and protein abundance by Western blotting and confocal microscopy. As a result, TAC treatment increased the mRNA and protein levels of Anxa7 in wild-type mice. Moreover, TAC increased heart weight to body weight ratio and the cardiac mRNA levels of αSka, Nppb, Col1a1, Col3a1 and Rcan1, effects more pronounced in anxa7(-/-) mice than in anxa7(+/+) mice. Silencing of Anxa7 in HL-1 cardiomyocytes significantly increased nuclear localization of Nfatc1. Furthermore, Anxa7 silencing increased NFAT-dependent transcriptional activity as well as αSka, Nppb, and Rcan1 mRNA levels both, under control conditions and following β-adrenergic stimulation by isoproterenol. These observations point to an important role of annexin A7 in the regulation of cardiac NFAT activity and hypertrophic response following cardiac stress conditions.


Annexin A7; HL-1 cardiomyocytes; NFAT; Pressure overload

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