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MiR-410-3p Facilitates Angiotensin II-induced Cardiac Hypertrophy by Targeting Smad7

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Journal Bioengineered
Date 2021 Dec 24
PMID 34951337
Citations 7
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Abstract

MicroRNAs (miRNAs) have emerged as important regulators in the development of cardiovascular diseases. miR-410-3p was shown to play a protective or detrimental role in the progression in cardiovascular events. However, the exact role and the underlying mechanism of miR-410-3p in cardiac hypertrophy have not been documented. The current work was aimed to determine the role and underlying mechanism of miR-410-3p on Angiotensin II (Ang II) induced cardiac hypertrophy. FITC-phalloidin staining was used for determination of cardiomyocyte surface area. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was performed to identify mRNA expression level of hypertrophic markers. Smad7 protein expression level was analyzed using Western blot. Dual-luciferase reporter assay was used to examine the regulatory function of miR-410-3p on Smad7. MiR-410-3p was found significantly up-regulated in Ang II-induced cardiac hypertrophy. MiR-410-3p inhibitor remarkably alleviated cardiomyocyte hypertrophic changes. Dual-luciferase reporter assay result indicated that miR-410-3p directly targeted Smad7 and miR-410-3p inhibitor effectively prevented Ang II triggered down-regulation of Smad7. Moreover, Smad7 overexpression significantly reversed the pro-hypertrophic effect of miR-410-3p. In summary, our findings revealed that miR-410-3p mediated Ang II-induced cardiac hypertrophy via targeting inhibition of Smad7.

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References
1.
Ramasamy S, Velmurugan G, Rekha B, Anusha S, Rajan K, Shanmugarajan S . Egr-1 mediated cardiac miR-99 family expression diverges physiological hypertrophy from pathological hypertrophy. Exp Cell Res. 2018; 365(1):46-56. DOI: 10.1016/j.yexcr.2018.02.016. View

2.
Li L, Zhang Y, Yang H, Wang Y . Long non-coding RNA FTX alleviates hypoxia/reoxygenation-induced cardiomyocyte injury via miR-410-3p/Fmr1 axis. Eur Rev Med Pharmacol Sci. 2020; 24(1):396-408. DOI: 10.26355/eurrev_202001_19938. View

3.
Wang Y, Zhen D, Fu D, Fu Y, Zhang X, Gong G . 1, 8-cineole attenuates cardiac hypertrophy in heart failure by inhibiting the miR-206-3p/SERP1 pathway. Phytomedicine. 2021; 91:153672. DOI: 10.1016/j.phymed.2021.153672. View

4.
Niu X, Huang B, Qiao X, Liu J, Chen L, Zhong M . MicroRNA-1-3p Suppresses Malignant Phenotypes of Ameloblastoma Through Down-Regulating Lysosomal Associated Membrane Protein 2-Mediated Autophagy. Front Med (Lausanne). 2021; 8:670188. PMC: 8187618. DOI: 10.3389/fmed.2021.670188. View

5.
Wang P, Luo L, Shen Q, Shi G, Mohammed A, Ni S . Rosuvastatin improves myocardial hypertrophy after hemodynamic pressure overload via regulating the crosstalk of Nrf2/ARE and TGF-β/ smads pathways in rat heart. Eur J Pharmacol. 2017; 820:173-182. DOI: 10.1016/j.ejphar.2017.12.013. View