Abstract
BACKGROUND As one of the crucial causes leading to cardiovascular disease, atherosclerosis (AS) develops in association with the dysfunction of vascular smooth muscle cells (VSMCs). However, the associated mechanism of the proliferation and migration in VSMCs requires further elucidation. MATERIAL AND METHODS Human VSMCs and ApoE-knockout (ApoE-/-) mice were used to establish AS cell and animal models, respectively. Expression levels of miR-188-3p and fibroblast growth factor 1 (FGF1) mRNA were detected using quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Western blot was used to assess FGF1 protein expression. The proliferation, migration, and apoptosis of the cells were determined using MTT, BrdU, and Transwell assays, as well as flow cytometry analysis. The interaction between miR-188-3p and FGF1 was validated using dual-luciferase reporter gene assay, qRT-PCR, and Western blot analysis. RESULTS MiR-188-3p was found to be significantly decreased in the serum of AS patients and ApoE-/- mice as well as VSMCs of ApoE-/- mice and human VSMCs treated with oxidized low-density lipoprotein. MiR-188-3p repressed the proliferation and migration of VSMCs but promoted apoptosis of VSMCs. The binding site between miR-188-3p and 3' untranslated region (3'-UTR) of FGF1 was identified, and FGF1 was verified as a target gene of miR-188-3p. Restoration of FGF1 reversed the effects of miR-188-3p on VSMCs. CONCLUSIONS MiR-188-3p suppresses the proliferation and migration of VSMCs and induces their apoptosis through targeting FGF1.