MiR-410-3p facilitates Angiotensin II–induced cardiac hypertrophy by targeting Smad7

Q: What is the clinical evidence from this study?

Population: Cardiac hypertrophy. Intervention: miR-410-3p inhibitor vs. Control (Ang II alone). Primary outcome: Cardiomyocyte hypertrophy (cell size and hypertrophic markers) (p=<0.01).

Guizhi Jia; Chunguang Liang; Wenhui Li; Hongliang Dai

doi:10.1080/21655979.2021.2009968

December 24, 2021BioengineeredOpen Access

MiR-410-3p facilitates Angiotensin II–induced cardiac hypertrophy by targeting Smad7

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Key result

MiR-410-3p facilitates Angiotensin II-induced cardiac hypertrophy by targeting and inhibiting Smad7, while its inhibition significantly alleviates cardiomyocyte hypertrophic changes.

Why the study?

The exact role and underlying mechanism of miR-410-3p in cardiac hypertrophy had not been documented.

Does miR-410-3p inhibition prevent Angiotensin II-induced cardiac hypertrophy in cardiomyocytes?

Key Points

To determine the biological role and underlying molecular mechanism of miR-410-3p in Angiotensin II–induced cardiac hypertrophy.
Assessed cardiomyocyte surface area using FITC-phalloidin staining following Angiotensin II (Ang II) stimulation.
Quantified mRNA expression of hypertrophic markers by qRT-PCR and evaluated Smad7 protein levels via Western blot.
Confirmed direct binding between miR-410-3p and Smad7 using dual-luciferase reporter assays combined with miR-410-3p inhibition and Smad7 overexpression.
MiR-410-3p was significantly upregulated in Ang II–induced hypertrophic cardiomyocytes, while its inhibition markedly alleviated hypertrophic changes.
Smad7 was identified as a direct target of miR-410-3p, with miR-410-3p inhibitors effectively preventing Ang II–mediated downregulation of Smad7.
Smad7 overexpression significantly reversed the pro-hypertrophic effects driven by miR-410-3p.

Structured PICO

Does miR-410-3p inhibition prevent Angiotensin II-induced cardiac hypertrophy in cardiomyocytes?

P

Population

In vitro study using primary cultures of neonatal rat ventricular myocytes to investigate the role of miR-410-3p in Angiotensin II-induced cardiac hypertrophy.

I

Intervention

miR-410-3p inhibitor and Smad7 overexpression

C

Comparator

Control / Angiotensin II alone

O

Outcome

Cardiomyocyte hypertrophic changes (surface area and mRNA expression of hypertrophic markers)surrogate

Main Result

p-value: p=<0.01

Inhibition of miR-410-3p alleviates Angiotensin II-induced cardiac hypertrophy by targeting Smad7, suggesting a potential therapeutic target for cardiac hypertrophy.

Limitations

The study only confirmed the in vitro mediating effect of miR-410-3p on Ang II triggered cardiac hypertrophy.
Future work is required to confirm findings via in vivo animal studies and clinical assessment.

Implication

MiR-410-3p inhibition merits further preclinical testing in hypertrophy; leaves open any role in human cardiac disease.

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.

Discussion

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Published by Bioengineered · CC BY

Cite This Study

Jia et al. (2021) studied Cardiac hypertrophy. miR-410-3p inhibitor vs. Control (Ang II alone) was evaluated on Cardiomyocyte hypertrophy (cell size and hypertrophic markers) (p=<0.01). MiR-410-3p facilitates Angiotensin II-induced cardiac hypertrophy by targeting and inhibiting Smad7, while its inhibition significantly alleviates cardiomyocyte hypertrophic changes.

synapsesocial.com/papers/6a9df8cd031501fc02c7c8e4 https://doi.org/10.1080/21655979.2021.2009968

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MiR-410-3p facilitates Angiotensin II–induced cardiac hypertrophy by targeting Smad7

Key Points

Structured PICO

Main Result

Limitations

Implication

Abstract

Discussion

Figures from the paper

Cite This Study

MiR-410-3p facilitates Angiotensin II–induced cardiac hypertrophy by targeting Smad7

Key Points

Structured PICO

Main Result

Limitations

Implication

Abstract

Discussion

Figures from the paper

Cite This Study

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