Mir-24 regulates junctophilin-2 expression in cardiomyocytes.

ABSTRACT:

Rationale

Failing cardiomyocytes exhibit decreased efficiency of excitation-contraction (E-C) coupling. The downregulation of junctophilin-2 (JP2), a protein anchoring the sarcoplasmic reticulum to T-tubules, has been identified as a major mechanism underlying the defective E-C coupling. However, the regulatory mechanism of JP2 remains unknown.

Objective

To determine whether microRNAs regulate JP2 expression.

Methods and results

Bioinformatic analysis predicted 2 potential binding sites of miR-24 in the 3'-untranslated regions of JP2 mRNA. Luciferase assays confirmed that miR-24 suppressed JP2 expression by binding to either of these sites. In the aortic stenosis model, miR-24 was upregulated in failing cardiomyocytes. Adenovirus-directed overexpression of miR-24 in c

SUBMITTER: Xu M 

PROVIDER: S-EPMC3611051 | biostudies-literature | 2012 Sep

REPOSITORIES: biostudies-literature