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Article type: Research Article
Authors: Zhang, Yi-ming; * | Wang, Guo-hua | Xu, Miao-jun | Jin, Gan
Affiliations: Health Management Physical Examination Center, Shaoxing People’s Hospital, Shaoxing, Zhejiang, China
Correspondence: [*] Corresponding author: Yi-ming Zhang, Health Management Physical Examination Center, Shaoxing People’s Hospital, Shaoxing 312000, Zhejiang, China. E-mail: [email protected].
Abstract: OBJECTIVE: This study was designed to investigate the role of 8-oxoguanine DNA glycosylase 1 (OGG1) in preventing atherosclerosis-induced vascular EC injury, thereby providing a theoretical basis for the exploration of drug targets and treatment methods for atherosclerosis. METHODS: Human umbilical vein cell line (EA.hy926) was treated with ox-LDL to construct an in vitro atherosclerotic cell model. pcDNA3.1-OGG1 was transfected into EA.hy926 cells to overexpress OGG1. qRT-PCR, CCK-8 assay, flow cytometry, oil red O staining, ELISA, comet assay and western blot were used to evaluate the OGG1 expression, viability, apoptosis level, lipid droplet content, 8-OHdG level and DNA damage of cells in each group. RESULTS: Compared with the Control group, ox-LDL stimulation of endothelial cells significantly decreased cell viability, promoted apoptosis and DNA damage, and increased intracellular levels of 8-OHdG and γH2AX, while decreasing protein levels of PPARγ, FASN, FABP4, RAD51 and POLB. However, overexpression of OGG1 can significantly inhibit ox-LDL damage to endothelial cells, promote lipid metabolism, decrease lipid droplet content, and improve DNA repair function. CONCLUSION: Over-expression of OGG1 improves DNA repair. Briefly, OGG1 over-expression enhances the DNA damage repair of ECs by regulating the expression levels of γH2AX, RAD51 and POLB, thereby enhancing cell viability and reducing apoptosis.
Keywords: 8-oxoguanine DNA glycosylase 1 (OGG1), atherosclerosis, apoptosis, DNA damage repair
DOI: 10.3233/CH-232082
Journal: Clinical Hemorheology and Microcirculation, vol. 87, no. 2, pp. 249-261, 2024
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