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Detection of microRNA Expression in Peritoneal Membrane of Rats Using Quantitative Real-time PCR
Published on: June 27, 2017
MicroRNA-9 regulates cardiac fibrosis by targeting PDGFR-β in rats
Lei Wang1, LiKun Ma2, Hai Fan1
1Department of Cardiology, Anhui Provincial Hospital Affiliated to Anhui Medical University, No. 17 Lujiang Road, Hefei, 230001, China.
Abstract:
The proliferation of cardiac fibroblasts (CFs) and excessive deposition of extracellular matrix (ECM) are the main pathological characteristics of cardiac fibrosis. In recent years, microRNAs (miRNAs) have been found to be a new kind of regulator in cardiac fibrosis. The purpose of this study was to investigate the role of microRNA-9 (miR-9) in the process of cardiac fibrosis and its mechanism. Treatment of cultured neonatal rat CFs with PDGF-BB or serum suppressed the expression of miR-9. Overexpression of miR-9 obviously inhibited neonatal rat CFs proliferation and collagen production as detected by MTT assays, qRT-PCR, and western blotting. The effects of miR-9 in CFs were abrogated by co-transfection with miR-9 inhibitors. Overexpression of miR-9 reduced the mRNA and protein levels of PDGFR-βand its downstream protein, extracellular signal-regulated kinase (ERK) 1/2. Silencing PDGFR-βby small interfering RNA mimicked the anti-fibrotic action of miR-9, whereas overexpression of PGDFR-β canceled the effect of miR-9 in cultured CFs. Dual-luciferase reporter assays showed that PDGFR-βwas a direct target of miR-9. Overexpression of miR-9 inhibited cardiac fibrosis by targeting PDGFR-β, indicating that miR-9 might play a role in the treatment of cardiac fibrosis.
Insights
MicroRNA-9 (miR-9) inhibits cardiac fibroblast proliferation and collagen production, key factors in cardiac fibrosis. miR-9 targets PDGF receptor beta (PDGFR-β), suggesting a therapeutic role in treating cardiac fibrosis.
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- Biochemistry
Background:
- Cardiac fibrosis, characterized by fibroblast proliferation and excessive extracellular matrix deposition, is a major pathological feature of heart disease.
- MicroRNAs (miRNAs) have emerged as critical regulators in the pathogenesis of cardiac fibrosis.
Purpose of the Study:
- To investigate the role and mechanism of microRNA-9 (miR-9) in cardiac fibrosis.
- To explore miR-9's potential as a therapeutic target for cardiac fibrosis.
Main Methods:
- Neonatal rat cardiac fibroblasts (CFs) were treated with PDGF-BB or serum to modulate miR-9 expression.
- Overexpression and inhibition of miR-9 were performed using transfection techniques.
- Cell proliferation and collagen production were assessed using MTT assays, qRT-PCR, and western blotting.
- PDGF receptor beta (PDGFR-β) and ERK1/2 levels were analyzed.
- Dual-luciferase reporter assays were used to confirm direct targeting of PDGFR-β by miR-9.
Main Results:
- PDGF-BB or serum treatment suppressed endogenous miR-9 expression in CFs.
- Overexpression of miR-9 significantly inhibited CF proliferation and collagen production.
- miR-9 overexpression reduced PDGFR-β and ERK1/2 expression.
- Silencing PDGFR-β mimicked miR-9's anti-fibrotic effects, while PDGFR-β overexpression abrogated them.
- PDGFR-β was identified as a direct target of miR-9.
Conclusions:
- miR-9 acts as a negative regulator of cardiac fibroblast proliferation and extracellular matrix production.
- miR-9 exerts its anti-fibrotic effects by directly targeting PDGFR-β.
- miR-9 represents a potential therapeutic strategy for mitigating cardiac fibrosis.
