miR-26a在血管钙化中的作用机制

被引：1
|
作者：
吴伟
尚玉强
程龙
王杰
杨传蕾
机构：
[1] 华中科技大学同济医学院附属武汉中心医院心脏大血管外科
来源：
中国老年学杂志 | 2024年 / 44卷 / 04期
关键词：
miR-26a; 骨保护素(OPG)/核因子κB受体激活剂(RANK)/细胞核因子κB受体活化因子配体(RANKL)信号通路; 血管钙化;
D O I：
暂无
中图分类号：
R363 [病理生理学];
学科分类号：
摘要：
目的 探讨血管钙化过程中miR-26a表达差异及其作用机制。方法 通过体内和体外实验构建血管钙化模型，利用分子生物学、病理生物学及细胞生物学检测方法，验证血管钙化过程中miR-26a表达差异及可能作用机制。结果 与模型组和mimic NC组相比较，miR-26a mimic组碱性磷酸酶活性显著降低(P<0.05)。而inhibitor NC组和miR-26a inhibitor组碱性磷酸酶无显著变化(P>0.05)。与mimic NC组比较，miR-26a mimic组miR-26a、骨保护素(OPG)表达水平显著升高(P<0.05),而骨桥蛋白(OPN)、骨形态发生蛋白(BMP)-2和胶原蛋白(Collagen)Ⅱ表达水平显著降低(P<0.05)。与inhibitor NC组比较，miR-26a inhibitor组miR-26a、OPG、OPN、BMP-2和CollagenⅡ表达水平无显著差异(P>0.05)。结论 miR-26a在血管钙化中的作用机制可能与OPG/核因子κB受体激活剂(RANK)/细胞核因子κB受体活化因子配体(RANKL)信号通路有关。
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页码：893 / 896
页数：4
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