IRF2BP2 prevents ox‑LDL‑induced inflammation and EMT in endothelial cells via regulation of KLF2
- Yongri Jiang
- Qiuling Shen
Affiliations: Department of Cardiovascular Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China, Department of Laboratory Diagnosis, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China
- Published online on: March 12, 2021 https://doi.org/10.3892/etm.2021.9912
Copyright: © Jiang
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Oxidized low‑density lipoprotein (ox‑LDL)‑induced endothelial dysfunction contributes to the progression of atherosclerosis. Interferon regulatory factor 2‑binding protein 2 (IRF2BP2) attenuates macrophage‑mediated inflammation and susceptibility to atherosclerosis. However, the effects of IRF2BP2 on vascular endothelial cells in atherosclerosis have not been fully elucidated. In the present study, the effects of IRF2BP2 on cell viability, inflammation and endothelial‑to‑mesenchymal transition (EMT) of human umbilical vein endothelial cells (HUVECs) were assessed using Cell Counting Kit‑8 (CCK‑8) assays, ELISA kits and western blot analysis, respectively. In addition, the expression levels of Krüppel‑like factor 2 (KLF2) were determined by reverse transcription‑quantitative PCR and immunofluorescence assays. A Nitrate/Nitrite assay kit was utilized to detect the production of nitric oxide (NO). The results demonstrated that ox‑LDL induced inflammation and EMT of HUVECs, and decreased the NO levels. Furthermore, IRF2BP2 overexpression protected HUVECs against ox‑LDL‑induced inflammation, EMT and endothelial dysfunction, and resulted in upregulated expression of KLF2. Additionally, IRF2BP2 was shown to bind to KLF2, and KLF2 knockdown reversed the protective effects of IRF2BP2 on ox‑LDL‑exposed HUVECs. These findings indicated that IRF2BP2 may prevent ox‑LDL‑induced endothelial damage via upregulating KLF2 expression.