Key result
miR-183 overexpression attenuates cardiomyocyte hypertrophy in vitro by directly targeting TIAM1.
Why the study?
MiR-183 exhibits downregulated expression in cardiac hypertrophy, but its effect on cardiomyocyte hypertrophy remains to be examined.
Does miR-183 overexpression attenuate Angiotensin II-induced cardiomyocyte hypertrophy in vitro?
Does miR-183 overexpression attenuate Angiotensin II-induced cardiomyocyte hypertrophy in vitro?
miR-183 acts as a cardioprotective regulator against cardiomyocyte hypertrophy by directly targeting TIAM1, suggesting a potential therapeutic target for cardiac hypertrophy.
Should not yet change clinical practice; hypothesis-generating for miR-183/TIAM1 targeting in cardiac hypertrophy.
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.
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Gong et al. (2020) studied Cardiac hypertrophy. miR-183 mimic vs. negative control was evaluated on Cardiomyocytes size and prohypertrophic genes expression. Overexpression of miR-183 significantly attenuated cardiomyocyte hypertrophy and prohypertrophic gene expression in vitro by directly targeting TIAM1.
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