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  • Title: CircIRAK1 aggravates ox-LDL-induced endothelial cell injury in atherosclerosis via TRIM14 upregulation by binding to miR-330-5p.
    Author: Liu F, Gao B, Wang Y.
    Journal: Clin Hemorheol Microcirc; 2023; 85(3):195-209. PubMed ID: 36336926.
    Abstract:
    BACKGROUND: Atherosclerosis (AS) is a common inflammatory cardiovascular disease, and circular RNAs (circRNAs) are associated with the pathogenesis of AS. CircRNA Interleukin (IL)-1 receptor-associated kinase 1 (circIRAK1, hsa_circ_0091822) was upregulated in AS. The aims of this study were to ascertain the function and mechanism of circIRAK1 in AS. METHODS: Human Umbilical Vein Endothelial Cells (HUVECs) were treated with oxidized low-density lipoprotein (ox-LDL). RNA expression was detected by reverse transcription-quantitative polymerase chain reaction assay. Cell viability was examined using Cell Counting Kit-8 assay. Tube formation ability was measured by tube formation assay. Cell apoptosis was assessed using flow cytometry. Western blot was used for protein detection. Inflammatory reaction was evaluated via Enzyme-linked immunosorbent assay. Oxidative injury was analyzed by commercial kits. Target binding was determined through dual-luciferase reporter assay, RNA immunoprecipitation assay and pull-down assay. RESULTS: The expression of circIRAK1 was upregulated in AS serums and ox-LDL-treated HUVECs. Silencing circIRAK1 enhanced cell viability and angiogenesis while suppressed cell apoptosis, inflammatory response and oxidative stress in ox-LDL-stimulated HUVECs. CircIRAK1 served as a molecular sponge for miR-330-5p. CircIRAK1 regulated ox-LDL-mediated cell injury by absorbing miR-330-5p. In addition, miR-330-5p prevented endothelial cell dysfunction caused by ox-LDL via targeting tripartite motif containing 14 (TRIM14). TRIM14 expression was upregulated by circIRAK1 through sponging miR-330-5p. CONCLUSION: These results suggested that circIRAK1 upregulated TRIM14 by interacting with miR-330-5p, consequently contributing to ox-LDL-induced endothelial cell injury in AS.
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