miR‑19a promotes vascular smooth muscle cell proliferation, migration and invasion through regulation of Ras homolog family member B.

Diabetic patients with high glucose exhibit vascular smooth muscle cell (VSMC) alteration. Thrombotic disease is related to erosion of an unstable plaque, the instability of which leads to ruptures, for example, a thin fibrous cap derived from VSMCs. VSMC proliferation, migration and invasion are related to thrombotic diseases, including atherosclerosis. MicroRNA‑19a (miR‑19a) has been reported to have pleiotropic functions in cancer cell survival, apoptosis and migration. The present study aimed to investigate the effect of miR‑19a on VSMC proliferation, migration and invasion, and its mechanism. Cell Counting Kit‑8 and a propidium iodide kit were used to determine the proliferation and cycle of VSMCs. A cell migration assay was performed by scratching and Matrigel was used in a cell invasion assay. miR‑19a binding to Ras homolog family member B (RHOB), and their protein and mRNA expressions were determined by performing a dual luciferase assay, western blotting and reverse transcription‑quantitative PCR, respectively. It was demonstrated that miR‑19a promoted the proliferation, migration and invasion of VSMCs, promoted the expressions of dual specificity phosphatase Cdc25A (CDC25A), cyclinD1, matrix metalloproteinase (MMP)‑2, MMP‑9, α‑smooth muscle actin (α‑SMA) and smooth muscle 22α (SM22α), and inhibited suppressor of cytokine signaling 3 and RHOB expressions in VSMCs, while miR‑19a had no effect on the expression of T‑cell intracellular antigen‑1. The miR‑19a site bound to the RHOB gene position and inhibited RHOB to promote VSMC proliferation, invasion and migration, and increased MMP‑2, MMP‑9, α‑SMA and SM22α expressions. The present study suggested that miR‑19a could promote VSMC proliferation, migration and invasion via the cyclinD1/CDC25A and MMP/α‑SMA/SM22α signaling pathways. Moreover, miR‑19a promoted proliferation, migration and invasion via the MMP/α‑SMA/SM22α signaling pathway by inhibiting RHOB, suggesting that miR‑19a is a possible regulatory factor of RHOB.

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