MicroRNA-183 as a Novel Regulator Protects Against Cardiomyocytes Hypertrophy via Targeting TIAM1

医学 转染 小RNA 荧光素酶 报告基因 发病机制 血管紧张素II 心肌细胞 基因表达 信使核糖核酸 表型 调节器 细胞生物学 下调和上调 肌肉肥大 内科学 内分泌学 癌症研究 基因 生物 遗传学 受体
作者
Fu‐Han Gong,Xi-Lu Chen,Quan Zhang,Xiao-Qiang Xiao,Yongsheng Yang,Bian-jing Song,Sheng-ping Chao,Wen‐Lin Cheng
出处
期刊:American Journal of Hypertension [Oxford University Press]
卷期号:35 (1): 87-95 被引量:8
标识
DOI:10.1093/ajh/hpaa144
摘要

MicroRNAs serve as important regulators of the pathogenesis of cardiac hypertrophy. Among them, miR-183 is well documented as a novel tumor suppressor in previous studies, whereas it exhibits a downregulated expression in cardiac hypertrophy recently. The present study was aimed to examine the effect of miR-183 on cardiomyocytes hypertrophy.Angiotensin II (Ang II) was used for establishment of cardiac hypertrophy model in vitro. Neonatal rat ventricular cardiomyocytes transfected with miR-183 mimic or negative control were further utilized for the phenotype analysis. Moreover, the bioinformatics analysis and luciferase reporter assays were used for exploring the potential target of miR-183 in cardiomyocytes.We observed a significant decreased expression of miR-183 in hypertrophic cardiomyocytes. Overexpression of miR-183 significantly attenuated the cardiomyocytes size morphologically and prohypertrophic genes expression. Moreover, we demonstrated that TIAM1 was a direct target gene of miR-183 verified by bioinformatics analysis and luciferase reporter assays, which showed a decreased mRNA and protein expression in the cardiomyocytes transfected with miR-183 upon Ang II stimulation. Additionally, the downregulated TIAM1 expression was required for the attenuated effect of miR-183 on cardiomyocytes hypertrophy.Taken together, these evidences indicated that miR-183 acted as a cardioprotective regulator for the development of cardiomyocytes hypertrophy via directly regulation of TIAM1.
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