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MicroRNA-124 inhibits macrophage cell apoptosis via targeting p38/MAPK signaling pathway in atherosclerosis development

机译:MicroRNA-124通过靶向P38 / MAPK信号通路在动脉粥样硬化发育中抑制巨噬细胞细胞凋亡

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摘要

The objective of this study is to characterize the function of microRNA (miR)-124 in the process of coronary artery disease (CAD). Eighty patients, including 40 CAD patients and 40 non-CAD control patients were enrolled in this study. Atherosclerosis model was established in -/- mice and in RAW264.7 cells. Expression of miR-124 and p38 in patients, animal models and cell models were measured by qRT-PCR, western blot and immunohistochemistry assay. Overexpression or suppression of miR-124 was introduced and and the expression levels of p38, miR-124, pro- and anti-inflammatory cytokines, and pro- and anti-apoptotic factors were examined. Results showed that miR-124 was decreased, while p38 was increased in CAD patients and atherosclerosis models compared with control group. MiR-124 could target p38 by binding its 3’ untranslated region and negatively regulated the protein expression of p38. Overexpression of miR-124 increased the expression of anti-inflammatory cytokines, reduced the expression of pro- inflammatory cytokines, and inhibited macrophage apoptosis. MiR-124 overexpression may be a promising treatment for atherosclerosis and CAD via inhibiting p38.
机译:本研究的目的是在冠状动脉疾病(CAD)过程中表征MicroRNA(miR)-124的功能。本研究报告了八十名患者,其中包括40名CAD患者和40名非CAD对照患者。在/ - 小鼠和RAW264.7细胞中建立了动脉粥样硬化模型。 MiR-124和P38在患者中,动物模型和细胞模型的表达是通过QRT-PCR,Western印迹和免疫组织化学测定的。引入了MiR-124的过表达或抑制,并检查了P38,miR-124,促炎细胞因子和抗凋亡因子的表达水平。结果表明,与对照组相比,MIR-124减少,而P38增加了CAD患者和动脉粥样硬化模型。 MiR-124可以通过结合其3'未翻转区域来靶向P38,并对P38的蛋白质表达进行负调节。 miR-124的过表达增加了抗炎细胞因子的表达,降低了促炎细胞因子的表达,抑制巨噬细胞凋亡。 miR-124过表达可能是通过抑制p38的动脉粥样硬化和cad的有希望的治疗方法。

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