MicroRNA‑1 suppresses cardiac hypertrophy by targeting nuclear factor of activated T cells cytoplasmic 3.
|
| Abstract |
Cardiomyocyte hypertrophy is a threat to human health due to the probability of sudden heart failure‑induced mortality. Previous studies have demonstrated that nuclear factor of activated T cells cytoplasmic 3 (NFATC3) is important in the process of cardiomyocyte hypertrophy. However, the molecular mechanism underlying the alteration in the expression levels of NFATC3 during cardiomyocyte hypertrophy has remained to be fully elucidated. In order to shed light on the molecular mechanism, the present study employed several approaches, including the measurement of the cell surface area, analysis of the protein/DNA ratio, western blot analysis and a Luciferase reporter assay using isolated rat cardiomyocytes as model. The results showed that expression of microRNA‑1 (miR‑1) was reduced in patients diagnosed with cardiac hypertrophy and rat cardiomyocytes treated with pro‑hypertrophic stimuli. The increase in the expression of miR‑1 was able to inhibit the hypertrophic remodeling of cardiomyocytes. The suppression of miR‑1 was sufficient to induce cardiomyocyte hypertrophy, and further experiments confirmed that NFATC3 was a target of miR‑1 in cardiomyocytes. Forced expression of NFATC3 inhibited the protective activity of miR‑1 against hypertrophic stimuli in the cardiomyocytes. These findings provided clarification of the regulatory signaling pathway underlying cardiac hypertrophy, and provided evidence that targeting the miR‑1/NFATC3 pathway may be a promising strategy for the prevention and treatment of heart hypertrophy.
|
|---|---|
| Authors | Honglei Yin, Lihua Zhao, Shaoli Zhang, Yan Zhang, Suyang Lei |
| Journal | Molecular medicine reports (Mol Med Rep) Vol. 12 Issue 6 Pg. 8282-8 (Dec 2015) ISSN: 1791-3004 [Electronic] Greece |
| PMID | 26497337 (Publication Type: Journal Article) |
| Chemical References |
|
| Topics |
|
Join CureHunter, for free Research Interface BASIC access!
Realize the full power of the drug-disease research graph!