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Published on: June 3, 2018
LncRNA MHRT Promotes Cardiac Fibrosis via miR-3185 Pathway Following Myocardial Infarction
Mingjian Lang1, Dengke Ou1, Zhaohui Liu1
1Department of Cardiovascular Medicine, Chengdu Fifth People's Hospital.
Abstract:
Long-chain noncoding RNA (lncRNA) is a new class of molecular regulators in heart development and disease. However, the role of specific lncRNA in cardiac fibrosis remains to be fully explored. This study aimed to investigate the role and potential mechanism of lncRNA MHRT in myocardial fibrosis after myocardial infarction (MI).Cardiac fibroblasts (CFs) were isolated from a mouse model of MI. The expression levels of MHRT and miR-3185 in the hearts of MI and CFs mice treated with transforming growth factor beta 1 (TGF-β1) were analyzed by qRT-PCR. The collagen expression was assessed using qRT-PCR and Western blot. Cell proliferation was assessed by performing MTT and EdU assays. The direct interaction between lncRNA and miRNA was analyzed by luciferase assay, RNA-binding protein immunoprecipitation (RIP) assay, and RNA pull-down assay.The expression levels of MHRT were raised in MI and CFs mice treated with TGF-β1. Overexpression of MHRT promoted collagen production and CF proliferation, while silencing of MHRT showed the opposite effect. MiR-3185 was a target gene of MHRT. In addition, overexpression of MHRT reduced the expression levels of miR-3185, and siMHRT reversed the inhibitory effect of TGF-β1 on the expression of miR-3185. Overexpression of miR-3185 inhibited the upregulation of Col I and Col III induced by TGF-β1.MHRT promoted cardiac fibrosis after MI through miR-3185 and increased myocardial collagen deposition and promoted myocardial fibrosis.
Insights
Long-chain noncoding RNA MHRT promotes cardiac fibrosis after myocardial infarction by regulating miR-3185. This mechanism increases collagen deposition and cell proliferation, contributing to heart disease progression.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- RNA Biology
Background:
- Long-chain noncoding RNAs (lncRNAs) are emerging regulators in cardiac development and disease.
- The specific roles of lncRNAs, like MHRT, in myocardial fibrosis post-myocardial infarction (MI) require further elucidation.
Purpose of the Study:
- To investigate the function and underlying mechanism of lncRNA MHRT in myocardial fibrosis following MI.
- To explore the interaction between MHRT and miR-3185 in the context of cardiac fibroblast activation.
Main Methods:
- Quantitative reverse transcription PCR (qRT-PCR) and Western blot to analyze gene and protein expression.
- Cell proliferation assays (MTT, EdU) to assess fibroblast activity.
- Luciferase, RNA-binding protein immunoprecipitation (RIP), and RNA pull-down assays to confirm molecular interactions.
Main Results:
- MHRT expression was upregulated in MI hearts and TGF-β1-treated cardiac fibroblasts (CFs).
- MHRT overexpression enhanced collagen production and CF proliferation, while MHRT silencing had opposing effects.
- MHRT directly targeted and downregulated miR-3185; miR-3185 overexpression inhibited TGF-β1-induced collagen expression.
Conclusions:
- lncRNA MHRT exacerbates cardiac fibrosis post-MI by modulating the miR-3185 pathway.
- MHRT contributes to increased myocardial collagen deposition and fibroblast proliferation, highlighting its potential as a therapeutic target.
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