| First Author | Voelkl J | Year | 2014 |
| Journal | Biochem Biophys Res Commun | Volume | 445 |
| Issue | 1 | Pages | 244-9 |
| PubMed ID | 24508799 | Mgi Jnum | J:218578 |
| Mgi Id | MGI:5617932 | Doi | 10.1016/j.bbrc.2014.01.186 |
| Citation | Voelkl J, et al. (2014) Annexin A7 deficiency potentiates cardiac NFAT activity promoting hypertrophic signaling. Biochem Biophys Res Commun 445(1):244-9 |
| abstractText | 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 alphaSka, 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 alphaSka, Nppb, and Rcan1 mRNA levels both, under control conditions and following beta-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. |
