通过AMPK/FOXO3信号通路,FOXO3保护透镜上皮细胞免受UVB诱导的氧化应激
Yang Sun1,2,3,4,5, Yingying Hong1,2,3,4, Li Ning1,2,3,4
1Eye Institute and Department of Ophthalmology, Eye & ENT Hospital, Fudan University, Shanghai, China.
概括
FOXO3蛋白通过减少氧化应激和亡来保护人类透镜细胞免受UVB损伤. 这种保护作用涉及AMPK/FOXO3通路和IncRNA SNHG12的调节,为与年龄相关的白内障提供了潜在的治疗.
科学领域:
- 眼科医生 眼科 眼科
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
背景情况:
- 与年龄相关的白内障 (ARC) 是导致视力丧失的主要原因,紫外线B (UVB) 辐射有助于透镜氧化损伤.
- FOXO3 是细胞对衰老,细胞亡和氧化应激反应的关键调节者.
研究的目的:
- 研究FOXO3在UVB诱导的人类镜片上皮细胞 (HLECs) 氧化应激中的作用和调节机制.
主要方法:
- 在白内障进展和UVB暴露模型中评估FOXO3表达.
- 在HLEC中使用FOXO3过度表达/敲击进行了功能性测试.
- 使用 luciferase 记者测试研究了AMPK/FOXO3 信号通路和 lncRNA SNHG12 相互作用.
主要成果:
- 随着白内障的进展和UVB照射,FOXO3的表达减少.
- 过度表达FOXO3通过增强活力,减少活性氧物种 (ROS) 和抑制亡来保护HLECs免受UVB诱导的损伤.
- 确定AMPK/FOXO3通路和FOXO3对lncRNA SNHG12的负调节是关键机制. 击SNHG12也减轻了UVB引起的损伤.
结论:
- 通过AMPK/FOXO3通路和SNHG12调节,FOXO3可以减轻UVB诱导的氧化应激和透镜上皮细胞的亡.
- 这些发现突出了FOXO3作为与年龄相关的白内障的潜在治疗点.
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