MiR-125b attenuates retinal pigment epithelium oxidative damage via targeting Nrf2/HIF-1α signal pathway

2022 ◽  
Vol 410 (1) ◽  
pp. 112955
Author(s):  
Jin-xia Liu ◽  
Dong-yue Ma ◽  
Xin-yu Zhi ◽  
Ming-wu Wang ◽  
Jiang-yue Zhao ◽  
...  
Keyword(s):  
Retinal Pigment Epithelium ◽  
Oxidative Damage ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Signal Pathway

scholarly journals High-glucose induces retinal pigment epithelium mitochondrial pathways of apoptosis and inhibits mitophagy by regulating ROS/PINK1/Parkin signal pathway

2019 ◽  
Vol 111 ◽  
pp. 1315-1325 ◽  
Author(s):  
Yuanping Zhang ◽  
Xiaoting Xi ◽  
Yan Mei ◽  
Xueying Zhao ◽  
Liqiong Zhou ◽  
...  
Keyword(s):  
Retinal Pigment Epithelium ◽  
High Glucose ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Signal Pathway

scholarly journals Heterochromatin protects retinal pigment epithelium cells from oxidative damage by silencing p53 target genes

2018 ◽  
Vol 115 (17) ◽  
pp. E3987-E3995 ◽  
Author(s):  
Lili Gong ◽  
Fangyuan Liu ◽  
Zhen Xiong ◽  
Ruili Qi ◽  
Zhongwen Luo ◽  
...  
Keyword(s):  
Retinal Pigment Epithelium ◽  
Oxidative Damage ◽  
Target Genes ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Critical Role ◽  
Age Related Macular Degeneration ◽  
Protective Function ◽  
Heterochromatin Formation ◽  
Age Related

Oxidative stress (OS)-induced retinal pigment epithelium (RPE) cell apoptosis is critically implicated in the pathogenesis of age-related macular degeneration (AMD), a leading cause of blindness in the elderly. Heterochromatin, a compact and transcriptional inert chromatin structure, has been recently shown to be dynamically regulated in response to stress stimuli. The functional mechanism of heterochromatin on OS exposure is unclear, however. Here we show that OS increases heterochromatin formation both in vivo and in vitro, which is essential for protecting RPE cells from oxidative damage. Mechanistically, OS-induced heterochromatin selectively accumulates at p53-regulated proapoptotic target promoters and inhibits their transcription. Furthermore, OS-induced desumoylation of p53 promotes p53–heterochromatin interaction and regulates p53 promoter selection, resulting in the locus-specific recruitment of heterochromatin and transcription repression. Together, our findings demonstrate a protective function of OS-induced heterochromatin formation in which p53 desumoylation-guided promoter selection and subsequent heterochromatin recruitment play a critical role. We propose that targeting heterochromatin provides a plausible therapeutic strategy for the treatment of AMD.

scholarly journals Differential Mechanisms of Action and Efficacy of Vitamin E Components in Antioxidant Cytoprotection of Human Retinal Pigment Epithelium

2022 ◽  
Vol 12 ◽  
Author(s):  
R. Scott Duncan ◽  
Daniel T. Hurtado ◽  
Conner W. Hall ◽  
Peter Koulen
Keyword(s):  
Oxidative Stress ◽  
Vitamin E ◽  
Retinal Pigment Epithelium ◽  
Oxidative Damage ◽  
Mechanism Of Action ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Similar Efficacy ◽  
Rpe Cells ◽  
Junction Protein

The purpose of this study was to determine if different vitamin E components exhibit similar efficacy and mechanism of action in protecting Retinal pigment epithelium (RPE) cells from oxidative damage. We hypothesized that α-tocopherol (αT) is unique among vitamin E components in its cytoprotective mechanism of action against oxidative stress in RPE cells and that it requires protein synthesis for optimal antioxidant effect. We used cell viability assays, fluorescent chemical labeling of DNA and actin and immuno-labeling of the antioxidant proteins Nrf2 and Sod2 and of the tight junction protein, ZO-1, and confocal microscopy to determine the effects of αT and γT against oxidative stress in immortalized human RPE cells (hTERT-RPE). Using the four main vitamin E components, αT, γT, δ-tocopherol (δT) and α-tocotrienol (αTr), we ascertained that they exhibit similar, but not identical, antioxidant activity as αT when used at equimolar concentrations. In addition, we determined that the exposure time of RPE cells to α-tocopherol is critical for its ability to protect against oxidative damage. Lastly, we determined that αT, but not γT, partially requires the synthesis of new proteins within a 24-h period and prior to exposure to tBHP for optimal cytoprotection. We conclude that, unlike γT and δT, αT appears to be unique in its requirement for transport and/or signaling for it to be an effective antioxidant. As a result, more focus should be paid to which vitamin E components are used for antioxidant interventions.

ID2 protects retinal pigment epithelium cells from oxidative damage through p -ERK1/2/ID2/NRF2

2018 ◽  
Vol 650 ◽  
pp. 1-13 ◽  
Author(s):  
Yuting Fan ◽  
Zixin Huang ◽  
Chongde Long ◽  
Jie Ning ◽  
Han Zhang ◽  
...  
Keyword(s):  
Retinal Pigment Epithelium ◽  
Oxidative Damage ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Retinal Pigment Epithelium Cells ◽  
Epithelium Cells

scholarly journals High-glucose Induces Retinal Pigment Epithelium Mitochondrial Pathways of Apoptosis and Inhibits Mitophagy by Regulating ROS/PINK1/Parkin Signal Pathway

2018 ◽  
Author(s):  
Yuanping Zhang ◽  
Xiaoting Xi ◽  
Yan Mei ◽  
Xueying Zhao ◽  
Liqiong Zhou ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Retinal Pigment Epithelium ◽  
High Glucose ◽  
Cell Apoptosis ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Signal Pathway ◽  
Ros Generation ◽  
Autophagy Inhibitor ◽  
Ros Scavengers

AbstractDiabetic retinopathy (DR) caused visual performance degradation seriously endangers human beings’ health, uncovering the underlying mechanism might shed light on the discovery of DR therapeutic treatments. In this study, we found that the effects of glucose on retinal pigment epithelium (RPE) varies in a dose dependent manner, high-glucose promotes ROS generation and cell apoptosis, inhibits mitophagy as well as proliferative abilities, while low-glucose induces ROS production and cell mitophagy, but has little impacts on cell apoptosis and proliferation. Of note, the toxic effects of high-glucose on RPE are alleviated by ROS scavengers and aggravated by autophagy inhibitor 3-methyladenine (3-MA) or mitophagy inhibitor cyclosporin A (CsA). High-glucose induced ROS generation is merely eliminated by ROS scavengers instead of mitophagy or autophagy inhibitor. We also proved that high-glucose inhibits cell proliferation and promotes cell apoptosis by regulating ROS mediated inhibition of mitophagy. In addition, mitophagy associated proteins PINK1 and Parkin are downregulated by high-glucose or hydrogen peroxide treatments, which are reversed by ROS scavengers. Of note, Knock-down of PINK1 decreases phospharylated Parkin instead of total Parkin levels in RPE. Intriguingly, high-glucose’s inhibiting effects on cell mitophagy as well as proliferation and its promoting effects on cell apoptosis are reversed by either PINK1 or Parkin overexpression. Therefore, we concluded that high-glucose promotes RPE apoptosis and inhibits cell proliferation as well as mitophagy by regulating oxidative stress mediated inactivation of ROS/PINKl/Parkin signal pathway.

scholarly journals MITF protects against oxidative damage-induced retinal degeneration by regulating the NRF2 pathway in the retinal pigment epithelium

Redox Biology ◽  
2020 ◽  
Vol 34 ◽  
pp. 101537
Author(s):  
Shuxian Han ◽  
Jianjun Chen ◽  
Jiajia Hua ◽  
Xiaojuan Hu ◽  
Shuhui Jian ◽  
...  
Keyword(s):  
Retinal Pigment Epithelium ◽  
Oxidative Damage ◽  
Retinal Degeneration ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Nrf2 Pathway
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