MicroRNA-183 as a Novel Regulator Protects Against Cardiomyocytes Hypertrophy via Targeting TIAM1
| Autor: | Xi-Lu Chen, Sheng-Ping Chao, Yong-Sheng Yang, Quan Zhang, Xiao-Qiang Xiao, Wen-Lin Cheng, Bian-Jing Song, Fu-Han Gong |
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| Rok vydání: | 2020 |
| Předmět: |
Heart Ventricles
Regulator Cardiomegaly Muscle hypertrophy Pathogenesis 03 medical and health sciences 0302 clinical medicine microRNA Internal Medicine Animals Medicine Myocytes Cardiac T-Lymphoma Invasion and Metastasis-inducing Protein 1 030304 developmental biology 0303 health sciences Messenger RNA business.industry Angiotensin II Transfection Phenotype Rats Cell biology MicroRNAs Gene Expression Regulation 030220 oncology & carcinogenesis business |
| Zdroj: | American Journal of Hypertension. 35:87-95 |
| ISSN: | 1941-7225 0895-7061 |
| DOI: | 10.1093/ajh/hpaa144 |
| Popis: | BACKGROUND 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. METHODS 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. RESULTS 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. CONCLUSIONS Taken together, these evidences indicated that miR-183 acted as a cardioprotective regulator for the development of cardiomyocytes hypertrophy via directly regulation of TIAM1. |
| Databáze: | OpenAIRE |
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