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
Autor: | Feifei Li, Yahui Chen, Zhiling He, Chuangchang Wang, Xiaoli Wang, Guangming Pan, Jiang yang Peng, Qiuxiong Chen, Xia Wang |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
Epithelial-Mesenchymal Transition
mir-6873-5p Bioengineering cerna Applied Microbiology and Biotechnology Histone Deacetylases Cell Movement Human Umbilical Vein Endothelial Cells Humans Cell Proliferation hsa_circ_0001879 Base Sequence hdac9 General Medicine RNA Circular Up-Regulation Lipoproteins LDL Repressor Proteins MicroRNAs Proteolysis Disease Progression circrna atherosclerosis Biomarkers TP248.13-248.65 Research Article Research Paper Biotechnology |
Zdroj: | Bioengineered, Vol 12, Iss 2, Pp 10420-10429 (2021) Bioengineered article-version (VoR) Version of Record |
ISSN: | 2165-5987 2165-5979 |
Popis: | 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. |
Databáze: | OpenAIRE |
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