hsa_circ_0058092 protects against hyperglycemia‑induced endothelial progenitor cell damage via miR‑217/FOXO3
- Jie Cheng
- Weiwei Hu
- Fenghui Zheng
- Yongfa Wu
- Maoquan Li
Affiliations: Department of Interventional and Vascular Surgery, Tenth People's Hospital of Tongji University, Guangzhou, Guangdong 510405, P.R. China, Institute of Tropical Medicine, Guangzhou University of Traditional Chinese Medicine, Guangzhou, Guangdong 510405, P.R. China, Department of Endocrinology and Metabolism, Tenth People's Hospital of Tongji University, Shanghai 200072, P.R. China
- Published online on: June 29, 2020 https://doi.org/10.3892/ijmm.2020.4664
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et al. This is an open access article distributed under the
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Circular RNAs (circRNAs) regulate the expression of genes that are critical for various biological and pathological processes. Previous studies have reported that the expression of hsa_circ_0058092 is decreased in patients with diabetes mellitus (DM); however, the specific role of this circRNA in DM is unknown. In the present study, endothelial progenitor cells (EPCs) were isolated and a decreased hsa_circ_0058092 expression was found under conditions of hyperglycemia (HG). The overexpression of hsa_circ_0058092 protected the EPCs against HG‑induced damage by preserving cell survival, proliferation, migration and angiogenic differentiation. The overexpression of hsa_circ_0058092 also decreased the HG‑induced increase in NADPH‑oxidase proteins and inflammatory cytokines. Further investigation revealed that the overexpression of hsa_circ_0058092 enhanced FOXO3 expression, which was mediated through the interaction with miR‑217. Furthermore, the upregulation of miR‑217 or the downregulation of FOXO3 abolished the protective effects of hsa_circ_0058092 against HG‑induced EPC damage. On the whole, these data suggest that hsa_circ_0058092 acts via the miR‑217/FOXO3 pathway to protect against EPCs HG‑induced damage, and to preserve the migration and angiogenesis of EPCs.