Abstract
Circular RNA (circRNA) is a novel subgroup of noncoding RNA in the human transcriptome playing a vital role in the atherosclerosis of cerebrovascular disease. However, the in-depth mechanism by which circRNA regulates the vascular smooth muscle proliferation and migration is still elusive. Here, a novel identified circRNA, circCHFR, was validated to be aberrantly overexpressed in the ox-LDL-induced vascular smooth muscle cell (VSMCs). Functionally, the circCHFR silencing by oligonucleotide transfection suppressed the proliferation and migration ability of VSMCs. Mechanically, bioinformatics tools and luciferase reporter assay state that circCHFR acts as a sponge of miR-370, and miR-370 targets the 3′ UTR of FOXO1. Furthermore, the transcription factor FOXO1 could bind with the promoter region of CCND1 mRNA and promote Cyclin D1 expression. In summary, this finding states the vital role of the circCHFR/miR-370/FOXO1/Cyclin D1 axis and provides a profound understanding about the circRNA in smooth muscle cells and atherosclerosis.
Highlights
In the pathogenesis of AS, the proliferation of vascular smooth muscle cells (VSMCs) is the typical high-probability event accompanied by the generation of collagen fibers and the accumulation of lipids.[5]
Microarray Analysis Unveils the Aberrantly Expressed circRNA in the ox-LDL-Induced VSMCs The ox-LDL was administrated to the VSMCs in vitro to simulate the abnormal lipid metabolism in the AS
The AS caused by multiple vasculopathy triggers severe cardiovascular disease, including coronary heart disease, cerebral infarction, and peripheral vascular disease
Summary
Atherosclerosis (AS) is one group of the most common vascular diseases and the main cause of cerebral infarction, stroke, and cerebral ischemia-reperfusion injury, characterized by lipid metabolic disorders and originated from the intima.[1,2,3,4] In the pathogenesis of AS, the proliferation of vascular smooth muscle cells (VSMCs) is the typical high-probability event accompanied by the generation of collagen fibers and the accumulation of lipids.[5]. Introns, or intergenic regions, and its covalent loop could resist the RNase in turn to maintain its tissue specificity and abundance.[10] Sun et al.[11] reported that circRNA circACTA2 acts as a sponge binding miR-548f-5p and targets 30 UTR of a-SMA mRNA, upregulating a-SMA levels. Chen et al.[12] reported that circRNA circWDR77 silencing significantly inhibited the proliferation and migration; miR-124 and fibroblast growth factor 2 (FGF-2) were downstream targets of circWDR77, forming the circWDR77-miR-124-FGF2 regulation. The vital role of circRNA in the vascular endothelial cells is increasingly important
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