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Hsa_circ_0008360 sponges miR-186-5p to target CCND2 to modulate high glucose-induced vascular endothelial dysfunction.

ABSTRACT: Vascular endothelial dysfunction is associated with the progress of many diseases. Circular RNAs (circRNAs) take part in the dysfunction of vascular endothelium. CircRNA hsa_circ_0008360 (circ_0008360) is dysregulated in high glucose-treated vascular endothelium, while the role and mechanism of circ_0008360 in high glucose-induced dysfunction remain unknown. Human umbilical vascular endothelium cells (HUVEC) were stimulated via high glucose. The abundances of circ_0008360, miR-186-5p and cyclin D2 (CCND2) were examined via quantitative real-time polymerase chain reaction or western blot. Vascular endothelial dysfunction was assessed via cell viability, apoptosis, migration and tube formation. The target relationship between miR-186-5p and circ_0008360 or CCND2 was analyzed via dual-luciferase reporter, RNA pull-down and RNA immunoprecipitation analyses. Circ_0008360 expression was enhanced in high-glucose-treated HUVEC. Circ_0008360 silence mitigated high glucose-induced suppression of viability, migration, tube formation, and increase in apoptosis in HUVEC. MiR-186-5p was sponged by circ_0008360, and miR-186-5p inhibition reversed the effect of circ_0008360 silence on high glucose-induced vascular endothelial dysfunction. MiR-186-5p alleviated high glucose-induced vascular endothelial dysfunction via targeting CCND2. CCND2 interference abolished the aggravated effect of circ_0008360 on high glucose-induced vascular endothelial dysfunction. Circ_0008360 knockdown attenuated high glucose-induced vascular endothelial dysfunction via regulating miR-186-5p and CCND2, indicating circ_0008360 might act as a target for the treatment of vascular endothelial dysfunction.Abbreviations: circRNAs, circular RNAs; HUVEC, human umbilical vascular endothelium cells; CCND2, cyclin D2; XPNPEP3, X-prolyl aminopeptidase 3; ceRNAs, competing endogenous RNAs; miRNAs, microRNAs; qRT-PCR, quantitative real-time polymerase chain reaction; RIP, RNA immunoprecipitation; HIF-1α, hypoxia inducible factor 1 alpha; TLR3, toll-like receptor 3; AKAP12, A-Kinase Anchoring Protein 12; ox-LDL, oxidized low-density lipoprotein; HG, high glucose; NG, normal glucose.

SUBMITTER: Zhu QQ

PROVIDER: S-EPMC8344795 | biostudies-literature | 2021 Jul

REPOSITORIES: biostudies-literature

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Hsa_circ_0008360 sponges miR-186-5p to target CCND2 to modulate high glucose-induced vascular endothelial dysfunction.

Zhu Qian-Qian QQ Pu Xi-Bin XB Chen Tian-Chi TC Qiu Chen-Yang CY Wu Zi-Heng ZH Tian Lu L He Yang-Yan YY Wang Xiao-Hui XH Shang Tao T Wang Xun X Xiang Yi-Lang YL Li Dong-Lin DL Zhang Hong-Kun HK

Cell cycle (Georgetown, Tex.) 20210705 14

Vascular endothelial dysfunction is associated with the progress of many diseases. Circular RNAs (circRNAs) take part in the dysfunction of vascular endothelium. CircRNA hsa_circ_0008360 (circ_0008360) is dysregulated in high glucose-treated vascular endothelium, while the role and mechanism of circ_0008360 in high glucose-induced dysfunction remain unknown. Human umbilical vascular endothelium cells (HUVEC) were stimulated via high glucose. The abundances of circ_0008360, miR-186-5p and cyclin ...[more]

PMID: 34223793

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Project description:Hyperglycemia exposure results in the dysfunction of endothelial cells (ECs) and the development of diabetic complications. Circular RNAs (circRNAs) have been demonstrated to play critical roles in EC dysfunction. The current study aimed to explore the role and mechanism of circRNA CLIP-associating protein 2 (circ_CLASP2, hsa_circ_0064772) on HG-induced dysfunction in human umbilical vein endothelial cells (HUVECs). Quantitative real-time polymerase chain reaction (qRT-PCR) was used to assess the levels of circ_CLASP2, miR-140-5p and F-box, and WD repeat domain-containing 7 (FBXW7). The stability of circ_CLASP2 was identified by the actinomycin D and ribonuclease (RNase) R assays. Cell colony formation, proliferation, and apoptosis were measured by a standard colony formation assay, colorimetric 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl-2H-tetrazolium bromide (MTT) assay, and flow cytometry, respectively. Western blot analysis was performed to determine the expression of related proteins. Targeted correlations among circ_CLASP2, miR-140-5p, and FBXW7 were confirmed by dual-luciferase reporter assay. High glucose (HG) exposure downregulated the expression of circ_CLASP2 in HUVECs. Circ_CLASP2 overexpression or miR-140-5p knockdown promoted proliferation and inhibited apoptosis of HUVECs under HG conditions. Circ_CLASP2 directly interacted with miR-140-5p via pairing to miR-140-5p. The regulation of circ_CLASP2 overexpression on HG-induced HUVEC dysfunction was mediated by miR-140-5p. Moreover, FBXW7 was a direct target of miR-140-5p, and miR-140-5p regulated HG-induced HUVEC dysfunction via FBXW7. Furthermore, circ_CLASP2 mediated FBXW7 expression through sponging miR-140-5p. Our current study suggested that the overexpression of circ_CLASP2 protected HUVEC from HG-induced dysfunction at least partly through the regulation of the miR-140-5p/FBXW7 axis, highlighting a novel therapeutic approach for the treatment of diabetic-associated vascular injury.

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Hsa_circ_0008360 sponges miR-186-5p to target CCND2 to modulate high glucose-induced vascular endothelial dysfunction.

Publications

Hsa_circ_0008360 sponges miR-186-5p to target CCND2 to modulate high glucose-induced vascular endothelial dysfunction.

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