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Expression of miRNA-155 in carotid atherosclerotic plaques of apolipoprotein E knockout (ApoE −/− ) mice and the interventional effect of rapamycin

自噬 PI3K/AKT/mTOR通路 载脂蛋白E 小RNA 发病机制 炎症 癌症研究 免疫印迹 生物 细胞生物学 医学 信号转导 病理 免疫学 基因 细胞凋亡 疾病 生物化学
作者
Juanjuan Ma,Shaonan Yang,Aijun Ma,Xudong Pan,Hongliang Wang,Na Li,Shihai Liu,Mei Wu
出处
期刊:International Immunopharmacology [Elsevier]
卷期号:46: 70-74 被引量:23
标识
DOI:10.1016/j.intimp.2017.02.026
摘要

Carotid atherosclerosis (AS) is an inflammatory process and is the primary pathogenesis of cerebrovascular disease. Many factors are responsible for development of atherosclerosis such as inflammation and autophagy. It is reported that microRNAs (miRNAs) could regulate the development of atherosclerosis through targeting autophagy-related genes. Many studies have demonstrated that miRNA-155 could regulate autophagy in macrophages or tumor cells. However, the role of miRNA-155 on autophagy in carotid plaques is not yet known. In this study, we explore the expression of miRNA-155 and autophagy-related proteins in carotid plaques of ApoE-/- mice and the interventional effect of rapamycin. We compared the expression of miRNA-155 and autophagy-related proteins between the control, model and rapamycin groups using qRT-PCR and western blot. Compared to the control group, we found the miRNA-155 and LC3-II expression was up-regulated (P<0.05), expression ratio of phosphorylated mammalian target of rapamycin to total mammalian target of rapamycin (p-mTOR/mTOR) was down-regulated in model group (P<0.05), but atherosclerotic lesions were still aggravated. These results following rapamycin group indicated that miRNA-155 and LC3-II expression was significantly up-regulated (P<0.05), the expression ratio of p-mTOR/mTOR was significantly down-regulated (P<0.05), and atherosclerotic lesions were reduced. Our results showed in the early stages of atherosclerotic plaques development, effective autophagy could attenuate atherosclerosis in ApoE-/- mice. Furthermore, our results also demonstrated that rapamycin might promote the activation of the autophagy by enhancing the expression of miRNA-155, which delays the development of atherosclerotic plaques.
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