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KMID : 1094720230280010101
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Biotechnology and Bioprocess Engineering
2023 Volume.28 No. 1 p.101 ~ p.111
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Circ_0005280 Protects Human Lens Epithelial Cells against H2O2-induced Apoptosis and Oxidative Stress though miR-326/PLCD3 Axis
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Yanxia Zhu
Yan Cheng
Linli Ma
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Abstract
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Circular RNAs have been revealed to play a vital role in the pathogenesis of ocular diseases. Herein, the goal of this work was to investigate the role of circ_0005280 in the development of age-related cataract (ARC). Levels of genes and proteins were detected by quantitative realtime polymerase chain reaction and Western blot. SRA01/04 cells in experimental group were exposed to hydrogen peroxide (H2O2). Cell survival was analyzed using cell counting kit-8 assay, EDU (5-ethynyl-2′-deoxyuridine) assay, flow cytometry, and Western blot, respectively. The levels of glutathione (GSH) and superoxide dismutase (SOD) were detected using commercial kits. The dual-luciferase reporter assay was used to identify the target relationship between miR-326 and circ_0005280 or PLCD3 (phospholipase C Delta 3). Circ_0005280 was lowly expressed in lenses of ARC patients and H2O2-induced SRA01/04 cells. Circ_0005280 up-regulation attenuated H2O2-evoked oxidative stress evidenced by the reduction of GSH and SOD, inhibition of cell proliferation, and promotion of cell apoptosis in SRA01/04 cells. Mechanistically, circ_0005280 directly targeted miR-326 to up-regulate the expression of its target PLCD3. Further rescue experiments suggested that miR-326 overexpression reversed the inhibitory effects of circ_0005280 on H2O2-stlimualted SRA01/04 cell injury. Moreover, miR-326 inhibition led to the inhibition of cell death and oxidative stress in H2O2-chanllgended SRA01/04 cells, which were abolished by PLCD3 up-regulation. Circ_0005280 protected human lens epithelial cells against H2O2-induced apoptosis and oxidative stress though miR-326/PLCD3 axis, suggesting a novel insight into the pathology of ARC.
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KEYWORD
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circ_0005280, miR-326, phospholipase C Delta 3, human lens epithelial cells, oxidative stress, ARC
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