Microrna-133b aggravates atherosclerosis by activating the notch signaling pathway

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.