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

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.
AuthorsGuizhi Jia, Chunguang Liang, Wenhui Li, Hongliang Dai
JournalBioengineered (Bioengineered) Vol. 13 Issue 1 Pg. 119-127 (01 2022) ISSN: 2165-5987 [Electronic] United States
PMID34951337 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • 3' Untranslated Regions
  • MIRN410 microRNA, rat
  • MicroRNAs
  • Smad7 Protein
  • Smad7 protein, rat
  • Angiotensin II
Topics
  • 3' Untranslated Regions
  • Angiotensin II (adverse effects)
  • Animals
  • Cardiomegaly (chemically induced, genetics, metabolism)
  • Cells, Cultured
  • Disease Models, Animal
  • HEK293 Cells
  • Humans
  • MicroRNAs (genetics)
  • Myocytes, Cardiac (cytology, drug effects, metabolism)
  • Primary Cell Culture
  • Rats
  • Smad7 Protein (genetics, metabolism)
  • Up-Regulation

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