Abstract
The aim of the present study was to investigate the effect of miR‑133b on atherosclerosis (AS). A mouse model of AS (AS group) was established, and serum levels of total cholesterol, triglyceride, high‑density lipoprotein cholesterol and low‑density lipoprotein (LDL) cholesterol were detected. The thoracic aorta tissues were subjected to hematoxylin and eosin staining for pathological examination. Mice were intravenously injected with microRNA (miR)‑133b mimics (the miR‑133b mimic + AS group) and miR‑133b mimics negative control (the miR‑133b NC + AS group). Normal mice were named the Sham group. Vascular reconstruction parameters, the Collagen/Vascular Area Ratio (CA/CVA) and serum inflammatory factors of mice in each group were detected. mRNA expression was measured by reverse transcription‑quantitative PCR and protein expression was determined by western blot analysis. An in vitro model of AS was induced in vascular smooth muscle cells (VSMCs) using oxidized (ox)‑LDL. CCK‑8 and wound healing assays were used to detect cell proliferation and migration. Compared with the Sham group, mice of the AS group, the AS + miR‑133b NC group and the AS + miR‑133b mimic group had higher intima thickness (IT), tumor necrosis factor (TNF)‑α and monocyte chemoattractant protein (MCP)‑1 levels, as well as increased Notch1 and Jagged1 expression; and they had lower medial thickness (MT), CA/CVA ratio and Notch3 expression (all P<0.05). In addition, miR‑133b mimic promoted the proliferation and migration, upregulated Notch1 and Jagged1, and downregulated Notch3 in ox‑LDL‑induced VSMCs. Taken together, miR‑133b aggravates AS by activating the Notch signaling pathway, which could serve as a potential target for the treatment of AS.