MiR-338-5p ameliorates pathological cardiac hypertrophy by targeting CAMKII δ.

In this study, we first found that the regulation of miR-338-5p was aberrant in cardiac tissues of heart failure patients and transverse aortic constriction (TAC)-induced PCH mice. Overexpression of miR-338-5p in the heart using recombinant adeno-associated virus serotype 9 (rAAV9) ameliorated TAC-induced PCH, as indicated by a decreased heart weight/body weight (HW/BW) ratio. Furthermore, miR-338-5p mitigated the TAC-induced damage in heart contraction and relaxation function, as measured by echocardiography and a cardio hemodynamic measurement, respectively. We also identified CAMKIIδ as a direct target of miR-338-5p using bioinformatics tools and the luciferase reporter assay. Finally, we observed that the miR-338-5p-mediated downregulation of CAMKIIδ reversed the cell surface area enlargement induced by the Ang-II treatment in H9c2 cells. Therefore, we highlight a novel molecular mechanism of the miR-338-5p/CAMKIIδ axis that contributes to the pathogenesis of PCH. PMID: 31820396 [PubMed - as supplied by publisher]
Source: Archives of Pharmacal Research - Category: Drugs & Pharmacology Authors: Tags: Arch Pharm Res Source Type: research