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Regulation of Autophagy by High Glucose in Human Retinal Pigment Epithelium

机译：高糖对人视网膜色素上皮细胞自噬的调节

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Background: Autophagy is a self-degradative process that is important for balancing sources of energy at critical times in development and in response to nutrient stress. Retinal pigment epithelium (RPE) works as the outer blood retina barrier and is vulnerable to energy stress-induced injury. However, the effect of high glucose treatment on autophagy is still unclear in RPE. Methods: Transmission electron microscopy was used to detect the generation of autophagosome. Small interfering RNA (siRNA) and MTT was used to determine the effect of autophagy on cell viability. Western blots and immunohistochemistry were used to detect the expression pattern of autophagic markers, including LC3 and p62. Results: High glucose treatment results in a significant increase in the generation of autophagosome and altered expression of LC3 and p62. High glucose-induced autophagy is independent of mTOR signaling, but is mainly regulated via ROS-mediated ER stress signaling. Conclusion: In the scenario of high glucose-induced oxidative stress, autophagy may be required for the removal of damaged proteins, and provide a default mechanism to prevent high glucose-induced injury in RPE.
机译：背景：自噬是一种自我降解的过程，对于在发育的关键时刻和应对营养胁迫方面平衡能量来源非常重要。视网膜色素上皮（RPE）可以作为视网膜的外血屏障，并且容易受到能量压力引起的损伤。然而，高糖治疗对自噬的影响在RPE中仍不清楚。方法：采用透射电子显微镜检测自噬体的产生。小干扰RNA（siRNA）和MTT用于确定自噬对细胞活力的影响。 Western印迹和免疫组化用于检测自噬标记物（包括LC3和p62）的表达模式。结果：高糖治疗导致自噬体的生成显着增加，LC3和p62的表达发生改变。高糖诱导的自噬独立于mTOR信号传导，但主要通过ROS介导的ER应激信号传导来调节。结论：在高葡萄糖诱导的氧化应激中，自噬可能需要去除受损的蛋白质，并为防止高葡萄糖诱导的RPE损伤提供了默认机制。

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