In vivo suppression of microRNA-24 prevents the transition toward decompensated hypertrophy in aortic-constricted mice.

In Vivo Suppression of MiR-24 Prevents the Transition toward Decompensated Hypertrophy in Aortic-constricted Mice

Microsoft Word - 300806-R1_PAP_01_10_13

Rationale: During the transition from compensated hypertrophy to heart failure, the signaling between L-type Ca 2+ channels (LCCs) in the cell membrane/T-tubules (TTs) and ryanodine receptors (RyRs) in the sarcoplasmic reticulum (SR) becomes defective, partially due to the decreased expression of a TT-SR anchoring protein, junctophilin-2 (JP2). MiR-24, a JP2 suppressing microRNA, is up-regulate...

Inhibition of mTOR signaling with rapamycin regresses established cardiac hypertrophy induced by pressure overload.

BACKGROUND Rapamycin is a specific inhibitor of the mammalian target of rapamycin (mTOR). We recently reported that administration of rapamycin before exposure to ascending aortic constriction significantly attenuated the load-induced increase in heart weight by approximately 70%. METHODS AND RESULTS To examine whether rapamycin can regress established cardiac hypertrophy, mice were subjected...

Comprehensive Microarray Analysis Identify Dysregulated MicroRNAs in Pressure Overload Affected Hearts

Background: MicroRNAs (miRNAs) are emerging as key regulators of cardiovascular development and disease, being involved in cardiac hypertrophy, fibrosis, remodeling and heart failure. Aortic stenosis is the most common valvular heart disease, and thus, we undertook a detailed analysis of differentially expressed miRNAs in this disease. Methods and Findings: We set up a model of aortic stenosis ...

Role of oxidative stress in the aortic constriction-induced ventricular hypertrophy in rat

Introduction:Severe abdominal aortic constriction above the renal arteries induces arterial hypertension above the stenotic site that is the cause of cardiac hypertrophy. Previous studies have shown that high blood pressure induces myocardial oxidative stress with conflicting results. In the present study, we assessed the effects of acute hypertension on the myocardial oxidative stress an...