小RNA
调节器
肌肉肥大
功能(生物学)
抑制器
细胞生物学
下调和上调
激酶
心肌肥大
生物
内科学
内分泌学
医学
基因
遗传学
作者
Juan He,Shan Jiang,Fenglan Li,Xue-jiao Zhao,Er-fu Chu,Meina Sun,Ming-Zi Chen,Hui Li
标识
DOI:10.2310/jim.0b013e3182819ac6
摘要
Background MicroRNAs (miRNAs) participate in the regulation of cardiac hypertrophy. However, it remains largely unknown as to how miRNAs are integrated into the hypertrophic program. Ca 2+ /calmodulin-dependent protein kinase II (CaMKII) is a hypertrophic signaling marker. It is not yet clear which miRNAs can regulate CaMKIIδ. Purpose In this study, we identified which miRNAs could regulate CaMKIIδ and how to regulate CaMKIIδ. Methods Through computational and expression analyses, miR-30b-5p was identified as a candidate regulator of CaMKIIδ. Quantitative expression analysis of hypertrophic models demonstrated significant down-regulation of miR-30b-5p compared with control groups. Luciferase reporter assay showed that miR-30b-5p could significantly inhibit the expression of CaMKIIδ. Moreover, through gain-of-function and loss-of-function approaches, we found miR-30b-5p could negatively regulate the expression of CaMKIIδ and miR-30b-5p was a regulator of cardiac hypertrophy. Conclusion Our study demonstrates that the expression of miR-30b-5p is down-regulated in cardiac hypertrophy, and restoration of its function inhibits the expression of CaMKIIδ, suggesting that miR-30b-5p may act as a hypertrophic suppressor.
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