LncRNA MHRT Promotes Cardiac Fibrosis via miR-3185 Pathway Following Myocardial Infarction

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.