MicroRNA-208a-3p participates in coronary heart disease by regulating the growth of hVSMCs by targeting BTG1

Human vascular smooth muscle cells (hVSMCs) are crucial in the progression of coronary heart disease (CHD). The present study aimed to investigate the role of microRNA-208a-3p (miR-208a-3p) in hVSMCs. Reverse transcription quantitative-PCR was performed to detect the levels of miR-208a-3p in the per...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Experimental and therapeutic medicine 2022-01, Vol.23 (1), p.71, Article 71
Hauptverfasser: Wang, Dong, Yan, Caiyun
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Human vascular smooth muscle cells (hVSMCs) are crucial in the progression of coronary heart disease (CHD). The present study aimed to investigate the role of microRNA-208a-3p (miR-208a-3p) in hVSMCs. Reverse transcription quantitative-PCR was performed to detect the levels of miR-208a-3p in the peripheral blood samples of patients with CHD and healthy volunteers. The results showed that miR-208a-3p was significantly upregulated in peripheral blood samples from patients with CHD compared with in healthy volunteers. Bioinformatics analysis and dual-luciferase reporter assays indicated that B-cell translocation gene 1 (BTG1) was a direct target gene of miR-208a-3p, and was downregulated in the peripheral blood samples of patients with CHD. Furthermore, this study also suggested that miR-208a-3p served an inhibitory role in the proliferation of hVSMCs, induced cell apoptosis, promoted the protein expression of Bax and reduced Bcl-2 protein expression; however, these effects were reversed by BTG1 silencing. In addition, the role of the PI3K/AKT pathway in mediating hVSMC apoptosis was examined via western blot analysis. Results indicated that inhibition of miR-208a-3p decreased phosphorylated (p)-AKT protein expression levels and the ratio of p-AKT/AKT in hVSMCs; however, BTG1-small interfering RNA abolished these effects. Taken together, these findings revealed that miR-208a-3p served a critical role in CHD development, regulating hVSMC function via targeting of BTG1, which was associated with the PI3K/AKT signaling pathway. Therefore, downregulated miR-208a-3p may serve as an ideal therapeutic target for CHD diagnosis and therapy.
ISSN:1792-0981
1792-1015
DOI:10.3892/etm.2021.10994