Jun Yang1,2. 1. General Department, The Affiliated People's Hospital of Ningbo University, Ningbo City, Zhejiang Province, China. yangjun_yj11@163.com. 2. School of Medicine, Zhejiang University, No.251 Baizhang East Road, Baizhang Avenue, Yinzhou District, Ningbo City, 315000, Zhejiang Province, China. yangjun_yj11@163.com.
Abstract
BACKGROUND: Atherosclerosis (AS) is a complex inflammatory disease of the arterial wall. Mmu_circ_0000271 was found to be aberrantly expressed in AS, but its function and mechanism in AS have not been reported. OBJECTIVE: This study investigated the role of mmu_circ_0000271 in AS. METHODS: Mmu_circ_0000271 were identified using UCSC website, RNase R treatment, and nuclear‑cytoplasmic extraction. And mouse vascular smooth muscle cells (VSMCs) were used to establish the AS cell model by treating oxidized low-density lipoprotein (ox-LDL, 50 μg/ml). Next, the expression of circ_0000271 in VSMCs was determined by quantitative real-time PCR. The effect of overexpressed or silenced circ_0000271 on ox-LDL-treated VSMCs viability, angiogenesis and invasion were detected by MTT, tube formation and transwell assays. The proteins expressions of proliferative and migratory markers were measured by western blot. After the target relationship predication between circ_0000271 and miR-5123, these experiments were performed again to evaluate the effect of miR-5123 inhibitor on AS model cells. RESULTS: Mmu_circ_0000271 was stably and highly expressed in ox-LDL-treated VSMCs, and its expression was enriched in the cell cytoplasm. Circ_0000271 overexpression further promoted the ox-LDL-induced viability, angiogenesis and invasion, as well as the proliferation- and migration-related proteins in VSMCs, whereas circ_0000271 knockdown had the opposite effect. Moreover, circ_0000271 was found to target miR-5123 and circ_0000271 overexpression suppressed its expression. And miR-5123 inhibitor was capable of reversing the effect of shcirc_0000271 on AS model cells. CONCLUSION: Mmu_circ_0000271 regulated ox-LDL-induced VSMC proliferation and migration through bind to miR-5123, and it could serve as a potential biomarker for AS.
BACKGROUND: Atherosclerosis (AS) is a complex inflammatory disease of the arterial wall. Mmu_circ_0000271 was found to be aberrantly expressed in AS, but its function and mechanism in AS have not been reported. OBJECTIVE: This study investigated the role of mmu_circ_0000271 in AS. METHODS: Mmu_circ_0000271 were identified using UCSC website, RNase R treatment, and nuclear‑cytoplasmic extraction. And mouse vascular smooth muscle cells (VSMCs) were used to establish the AS cell model by treating oxidized low-density lipoprotein (ox-LDL, 50 μg/ml). Next, the expression of circ_0000271 in VSMCs was determined by quantitative real-time PCR. The effect of overexpressed or silenced circ_0000271 on ox-LDL-treated VSMCs viability, angiogenesis and invasion were detected by MTT, tube formation and transwell assays. The proteins expressions of proliferative and migratory markers were measured by western blot. After the target relationship predication between circ_0000271 and miR-5123, these experiments were performed again to evaluate the effect of miR-5123 inhibitor on AS model cells. RESULTS: Mmu_circ_0000271 was stably and highly expressed in ox-LDL-treated VSMCs, and its expression was enriched in the cell cytoplasm. Circ_0000271 overexpression further promoted the ox-LDL-induced viability, angiogenesis and invasion, as well as the proliferation- and migration-related proteins in VSMCs, whereas circ_0000271 knockdown had the opposite effect. Moreover, circ_0000271 was found to target miR-5123 and circ_0000271 overexpression suppressed its expression. And miR-5123 inhibitor was capable of reversing the effect of shcirc_0000271 on AS model cells. CONCLUSION: Mmu_circ_0000271 regulated ox-LDL-induced VSMC proliferation and migration through bind to miR-5123, and it could serve as a potential biomarker for AS.