ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2018
[MicroRNA-199a-3p enhances expressions of fibrosis-associated genes through targeting Smad1 in mouse cardiac fibroblasts].
Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 3 citations in OpenAlex.
- Plasma extracellular vesicles-derived MicroRNAs as potential biomarkers in idiopathic pulmonary fibrosis.Respiratory research · 2026Article
- MiR-199a family members are differentially regulated during physiological and pathological cardiac hypertrophy.Frontiers in physiology · 2026Article
- Review
- Comprehensive analyses of the microRNA-messenger RNA-transcription factor regulatory network in mouse and human renal fibrosis.Frontiers in genetics · 2022Article
- [Olmesartan inhibits age-associated migration and invasion of human aortic vascular smooth muscle cells by upregulating miR-3133 axis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the role of miR-199a-3p in cardiac fibrosis and the potential target of miR-199a-3p.
methodsCardiac fibroblasts were isolated from C57BL/6 mice and cultured. The miR-199a-3p mimic and Smad1 siRNA were transiently transfected into the cardiac fibroblasts via liposome. Dual luciferase reporter assay was performed to confirm the interaction between miR-199a-3p and the 3'-UTR of Smad1. The expressions of Smad1 and fibrosis-related genes at the mRNA and protein levels in the cells after miR-199a-3p mimic transfection were determined using RT-qPCR and Western blotting, respectively. The expressions of Smad1, Smad3 and fibrosis-related genes at the protein level in cells transfected with miR-199a-3p mimic and Smad1 siRNA were detected using Western blotting.
resultsOver-expression of miR-199a-3p significantly increased the expression of cardiac fibrosis-related genes in cultured mouse cardiac fibroblasts. Dual luciferase reporter assay revealed the interaction of miR-199a-3p with the 3'-UTR of Smad1. The results of RT-qPCR and Western blotting confirmed that miR-199a-3p inhibited Smad1 expression at the post- transcriptional level. Transfection with miR-199a-3p mimic and siRNA-mediated Smad1 silencing consistently activated the Smad3 signaling pathway and enhanced the expressions of cardiac fibrosis-related genes in the cardiac fibroblasts.
conclusionsAs the target gene of miR-199a-3p, Smad1 mediates the pro-fibrotic effect of miR-199a-3p by activating the Smad3 signaling in cultured mouse cardiac fibroblasts.
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