Oxidative stress and mitochondrial dysfunction of retinal ganglion cells injury exposures in long-term blue light

蛋白激酶B 氧化应激 活力测定 细胞生物学 线粒体 医学 生物 信号转导 细胞 内分泌学 生物化学
作者
Kaihua Guo,Chen Huang,Wei Wang,Pei Zhang,Ying Li,Ziyuan Liu,Minshu Wang
出处
期刊:International Journal of Ophthalmology [Press of International Journal of Ophthalmology (IJO PRESS)]
卷期号:13 (12): 1854-1863 被引量:3
标识
DOI:10.18240/ijo.2020.12.03
摘要

AIM: To investigate the phototoxic effect of long-term excessive narrow-band blue light in staurosporine-induced differentiated retinal ganglion cells-5 (SSRGC-5). METHODS: SSRGC-5 cells were divided into two groups, blue light group (BL group) and control group. Cell viability was assessed by using CCK-8 assay. Metabolic profile analysis was performed by using Seahorse extracellular flux analyzer. Mitochondria ultrastructure were studied via transmission electron microscope (TEM). Mitochondria contents and oxidative stress was evaluated by flow cytometry. Western blotting was performed to monitor the changes in mitogen-activated protein kinases (MAPK) pathway and PI3K/AKT pathway. RESULTS: Blue light caused morphological changes of SSRGC-5 cells. The cell viability was significantly decreased from 3h in BL group. Intercellular ROS and mitochondrial superoxide levels were increased following blue light exposure. Metabolic profiling identified blue light induced SSRGC-5 cells to have severely compromised mitochondrial function. This was accompanied by impaired mitochondrial ultrastructure and remodeling, increased expression of the mitochondrial related proteins, and increased glycolysis as compensation. Moreover, the results showed that blue light induced higher expression of p-p38, p38, p-JNK, p-ERK, p-c-Jun, c-Jun, and p-AKT. CONCLUSION: These findings indicate that excessive narrow-band blue light induces oxidative stress and mitochondrial metabolic remodeling dysregulate in SSRGC-5 cells. Activated MAPK and AKT signaling pathways are involved in this process.
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