MiR-29c-3p inhibits proliferation and migration in rat primary cardiac fibroblasts via interacting with STAT3.

BACKGROUND: The aim of this study was to elucidate the influence and molecular mechanism of microRNA-29c-3p (miR-29c-3p) on cell functions of cardiac fibroblasts. METHODS: Rat primary cardiac fibroblasts were induced with high-level glucose (HG), followed by determination of miR-29c-3p and signal transducer and activator of transcription 3 (STAT3) levels. The regulatory effects of miR-29c-3p and STAT3 (AG490) on proliferative and migratory potentials in HG-induced cardiac fibroblasts were examined by cell counting kit-8 (CCK-8) and Transwell assay, respectively. The interaction between miR-29c-3p and STAT3 was assessed by bioinformatics analysis and dual-luciferase reporter assay. RESULTS: MiR-29c-3p was downregulated, and STAT3 was upregulated in HG-induced cardiac fibroblasts. HG induction stimulated proliferative and migratory potentials in cardiac fibroblasts, which were attenuated by overexpression of miR-29c-3p. STAT3 was the target gene binding miR-29c-3p. Application of AG490, the STAT3 inhibitor, was able to reverse the promoted proliferative and migratory potentials in HG-induced cardiac fibroblasts with miR-29c-3p knockdown. CONCLUSIONS: MiR-29c-3p weakens the over-proliferative and over-migratory potentials in HG-induced cardiac fibroblasts via inactivating the STAT3 signaling.

Circulating lncRNA MHRT predicts survival of patients with chronic heart failure.

BACKGROUND: It has been reported that lncRNA myosin heavy-chain-associated RNA transcripts (MHRT) can inhibit the apoptosis of cardiomyocytes. It is one of the major pathological changes leading to chronic heart failure. METHODS: The expression level of lncRNA MHRT was assessed by qRT-PCR. Diagnostic values of lncRNA MHRT for chronic heart failure were analyzed by ROC curve analysis. Cell apoptosis was detected by cell apoptosis assay. RESULTS: The results demonstrated that expression of lncRNA MHRT in plasma was down-regulated in patients with chronic heart failure compared to that in healthy people. Down-regulation of lncRNA MHRT distinguished chronic heart failure from healthy people. Over-expression of lncRNA MHRT inhibited the apoptosis of human cardiomyocyte cell line AC16 after H2O2 treatment. Follow-up study showed that chronic heart failure patients with lower expression levels of lncRNA MHRT had worse survival conditions compared to patients with higher expression levels of lncRNA MHRT. CONCLUSION: We concluded that circulating lncRNA MHRT might serve as a diagnostic and prognostic marker for chronic heart failure treatment.

Microparticles from Patients Undergoing Percutaneous Coronary Intervention Impair Vasodilatation by Uncoupling Endothelial Nitric Oxide Synthase.

OBJECTIVES: Percutaneous coronary interventions (PCIs) save countless acute myocardial infarction (AMI) patients. However, endothelial injury is still an inevitable complication. Circulating microparticles (MPs) play important roles in vascular dysfunction. Whether PCI affects function of MPs remains unclear. METHODS: MPs were obtained from AMI patients (n = 38) both preoperatively and 24 h after PCI, and healthy subjects (n = 20). MPs origins were tested by flow cytometry. Rat thoracic aortas were incubated with MPs to determine the effects of MPs on phosphorylation of endothelial nitric oxide synthase (eNOS), caveolin-1 expression, eNOS association with heat shock protein 90 (Hsp90), generation of nitric oxide (NO) and superoxide anion (O2), and endothelial-dependent vasodilatation. RESULTS: Compared with healthy subjects, MP concentrations increased in AMI patients. Undergoing PCI had no further effect on MPs concentration, but it results in increased endothelial-derived MPs proportion and decreased platelet-derived MP ratio. MPs from AMI patients decreased eNOS phosphorylation at Ser1177, increased eNOS phosphorylation at T495 and caveolin-1 expression, decreased eNOS association with Hsp90, decreased NO production but increased (O2) generation, damaged endothelial-dependent vasodilatation. All of these effects of MPs were strengthened by PCI. CONCLUSIONS: PCI further enhances the vascular injury effect of MPs. Circulating MPs may be a potential therapeutic target for patients undergoing PCI.