Magic™ Anti-SIRT4 (N-terminal) polyclonal antibody

Cardiac hypertrophy is an adaptive enlargement of the myocardium in response to overload pressure of heart. From abundant studies, a conclusion is drawn that many microRNAs (miRNAs) are associated with cardiac hypertrophy and heart failure. To investigate the role of microRNA-497 (miR-497) in myocardial hypertrophy, two models were established in this study from cell level to integral level. Cardiac hypertrophy was induced by using angiotensin II (Ang II) in vitro and was created by transverse abdominal aortic constriction (TAC) in vivo. There was a significant decrease expression of miR-497 in cardiac hypertrophy models. Moreover, overexpression of miR-497 inhibited myocardial hypertrophy both in vitro and in vivo without heart function variation. In addition, luciferase reporter assays demonstrated that Sirt4 was a direct target gene of miR-497. Taking together, our study indicates that miR-497 modulates cardiac hypertrophy by targeting Sirt4 and may serve as a potential therapeutic substance in the course.

Yeast silent information regulator 2 (SIR2) is involved in extension of yeast longevity by calorie restriction, and SIRT3, SIRT4, and SIRT5 are mammalian homologs of SIR2 localized in mitochondria. We have investigated the localization of these three SIRT proteins of mouse. SIRT3, SIRT4, and SIRT5 proteins were localized in different compartments of the mitochondria. When SIRT3 and SIRT5 were co-expressed in the cell, localization of SIRT3 protein changed from mitochondria to nucleus. These results suggest that the SIRT3, SIRT4, and SIRT5 proteins exert distinct functions in mitochondria. In addition, the SIRT3 protein might function in nucleus. (c) 2007 Elsevier Inc. All rights reserved.