The potential inhibitory effects of miR‑19b on vulnerable plaque formation via the suppression of STAT3 transcriptional activity.

Atherosclerotic plaque growth requires angiogenesis, and acute coronary syndrome (ACS) is usually triggered by the rupture of unstable atherosclerotic plaques. Previous studies have identified typically circulating microRNA (miRNA/miR) profiles in patients with ACS. miRNAs serve important roles in the pathophysiology of atherosclerotic plaque progression. The present study aimed to investigate the potential role and mechanism of miR‑19b in plaque stability. miRNA array data indicated that 28 miRNAs were differentially expressed in the plasma of patients with unstable angina (UA; n=12) compared with in control individuals (n=12), and miR‑19b exhibited the most marked upregulation. Circulating miR‑19b levels were further validated in another independent cohort, which consisted of 34 patients with UA and 24 controls, by quantitative polymerase chain reaction. Gene Ontology annotations of the predicted target genes of miR‑19b suggested that miR‑19b may be involved in endothelial cell (EC) proliferation, migration and angiogenesis, which was confirmed by Cell Counting kit‑8, wound healing and tube formation assays in the present study. Finally, the present study indicated that miR‑19b may suppress signal transducer and activator of transcription 3 (STAT3) tyrosine phosphorylation and transcriptional activity in ECs, as determined by western blot analysis and luciferase reporter assay. In conclusion, the present study revealed that increased miR‑19b expression may delay unstable plaque progression in patients with UA by inhibiting EC proliferation, migration and angiogenesis via the suppression of STAT3 transcriptional activity.