期刊
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
卷 33, 期 1, 页码 107-116出版社
KARGER
DOI: 10.1159/000356654
关键词
High glucose; Autophagy; ROS; ER stress
资金
- National Natural Science Foundation of China [81300241, 81371055]
- National clinical key construction project [(2012) 649]
- Medical Science and Technology Development Project Fund of Nanjing [ZKX 12047, YKK12207, YKK12208]
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. Copyright (C) 2014 S. Karger AG, Basel
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