期刊论文详细信息
Bioengineered
Hsa_circ_0001879 promotes the progression of atherosclerosis by regulating the proliferation and migration of oxidation of low density lipoprotein (ox-LDL)-induced vascular endothelial cells via the miR-6873-5p-HDAC9 axis
Yahui Chen1  Guangming Pan1  Chuangchang Wang1  Qiuxiong Chen1  Xiaoli Wang2  Jiang yang Peng2  Feifei Li2  Xia Wang2  Zhiling He2 
[1] The Second Affiliated Hospital of Guangzhou University of Chinese Medicine;Guangdong Provincial Hospital of Traditional Chinese Medicine;
关键词: atherosclerosis;    circrna;    hsa_circ_0001879;    hdac9;    mir-6873-5p;    cerna;   
DOI  :  10.1080/21655979.2021.1997224
来源: DOAJ
【 摘 要 】

Atherosclerosis (AS) is a typical vascular disease. Emerging evidence has shown that circRNAs play key roles in the progression of AS, but the potential function and underlying mechanism of hsa_circ_0001879 remains unknown. We detected the expression level of hsa_circ_0001879 was determined by qRT-PCR, and the proliferation rate and migration ability of HUVECs were measured by CCK-8 assay and Transwell assay, respectively. Proliferative markers and epithelium mesenchymal transition (EMT) markers were measured through immunoblotting. A dual luciferase activity assay was performed to detect the interaction between circRNAs, miRNAs, and mRNAs. Hsa_circ_0001879 was upregulated in AS patients. Hsa_circ_0001879 inhibited the proliferation and migration ability of Human umbilical vein endothelial cells (HUVECs). Hsa_circ_0001879 directly bound to miR-6873-5p and acted as a sponge. miR-6873-5p-induced HDAC9 mRNA degradation was inhibited by hsa_circ_0001879. Hsa_circ_0001879 decreased the proliferation and migration of HUVECs by inhibiting miR-6873-5p-induced HDAC9 degradation.

【 授权许可】

Unknown   

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