细胞凋亡
血管平滑肌
下调和上调
免疫印迹
细胞生长
转染
冠状动脉疾病
细胞
癌症研究
细胞生物学
动脉
平滑肌
生物
化学
医学
基因
内科学
生物化学
作者
Huangdong Dai,Naishi Zhao,Yue Zheng
标识
DOI:10.1097/fjc.0000000000001275
摘要
The purpose of this study was to investigate the effect of circLDLR on the proliferation and apoptosis of vascular smooth muscle cells (VSMCs) in coronary artery disease and its regulatory mechanism. The expression of KDM6A was detected by qRT-PCR or Western blot. VSMCs were transfected with miR-26-5p mimic/inhibitor or OE KDM6A. Cell proliferation and apoptosis were assessed. Luciferase reporter gene assays were used to examine interactions between miR-26-5p and KDM6A in VSMCs. Downregulation of circLDLR was associated with increased miR-26-5p in coronary artery disease tissues. In addition, circLDLR could inhibit cell proliferation and promote cell apoptosis by regulating miR-26-5p. Moreover, the overexpression of KDM6A reduced VSMCs proliferation and increased apoptosis in an miR-26-5p/circLDLR axis-dependent manner. CircLDLR modulates the proliferation and apoptosis of VSMCs through miR-26-5p/KDM6A axis.
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