PRDX6 Protects ARPE-19 Cells from Oxidative Damage via PI3K/AKT Signaling

Xu, Zhiyun; Wu, Guojiu; Zhao, Xueying; Zhou, Liqiong; Zhang, Hong; Li, Jinghua; Ma, Linkun; YuanPing, Zhang

doi:10.1159/000430186

Cited by 44 publications

(30 citation statements)

References 40 publications

(40 reference statements)

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“…5d, e). Zha et al reported that PRDX6 protects cells from oxidative damage via PI3K/AKT signaling [64]; this study, together with ours, suggested an intimate relationship between the antioxidant ability and the activation of CaMKKβ/AMPK and PI3K/AKT pathways.…”

Section: Discussionsupporting

confidence: 86%

The role of sodium hydrosulfide in attenuating the aging process via PI3K/AKT and CaMKKβ/AMPK pathways

et al. 2017

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Age-related dysfunction of the central auditory system, known as central presbycusis, is characterized by defects in speech perception and sound localization. It is important to determine the pathogenesis of central presbycusis in order to explore a feasible and effective intervention method. Recent work has provided fascinating insight into the beneficial function of H2S on oxidative stress and stress-related disease. In this study, we investigated the pathogenesis of central presbycusis and tried to explore the mechanism of H2S action on different aspects of aging by utilizing a mimetic aging rat and senescent cellular model. Our results indicate that NaHS decreased oxidative stress and apoptosis levels in an aging model via CaMKKβ and PI3K/AKT signaling pathways. Moreover, we found that NaHS restored the decreased activity of antioxidants such as GSH, SOD and CAT in the aging model in vivo and in vitro by regulating CaMKKβ and PI3K/AKT. Mitochondria function was preserved by NaHS, as indicated by the following: DNA POLG and OGG-1, the base excision repair enzymes in mitochondrial, were upregulated; OXPHOS activity was downregulated; mitochondrial membrane potential was restored; ATP production was increased; and mtDNA damage, indicated by the common deletion (CD), declined. These effects were also achieved by activating CaMKKβ/AMPK and PI3K/AKT signaling pathways. Lastly, protein homeostasis, indicated by HSP90 alpha, was strengthened by NaHS via CaMKKβ and PI3K/AKT. Our findings demonstrate that the ability to resist oxidative stress and mitochondria function are both decreased as aging developed; however, NaHS, a novel free radical scavenger and mitochondrial protective agent, precludes the process of oxidative damage by activating CaMKKβ and PI3K/AKT. This study might provide a therapeutic target for aging and age-related disease.

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Section: Discussionsupporting

confidence: 86%

The role of sodium hydrosulfide in attenuating the aging process via PI3K/AKT and CaMKKβ/AMPK pathways

et al. 2017

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“…The main difference between the two particles is that MI increased the expression of the pro‐apoptotic protein HTRA2 more than its counterpart did, while CR suppressed the expression of the anti‐apoptotic protein ANXA7 more than MI. Furthermore, only MI affected the expression of antioxidant proteins such as aldehyde dehydrogenase (ALDH1A1) and peroxiredoxin‐6 (PRDX6), which are known to protect cells from apoptotic cell death (Luo et al ., ; Zha et al ., ). These results suggested that the MI exposures might be triggering oxidative stress pathways as MI has been reported to cause oxidative stress and apoptosis in human bronchial epithelial cells (Antognelli et al ., ).…”

Section: Discussionmentioning

confidence: 97%

Responses of A549 human lung epithelial cells to cristobalite and α-quartz exposures assessed by toxicoproteomics and gene expression analysis

et al. 2016

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In this study, we used cytotoxicity assays, proteomic and gene expression analyses to examine the difference in response of A549 cells to two silica particles that differ in physical properties, namely cristobalite (CR) and α‐quartz (Min‐U‐Sil 5, MI). Cytotoxicity assays such as lactate dehydrogenase release, 5‐bromo‐2′‐deoxyuridine incorporation and cellular ATP showed that both silica particles could cause cell death, decreased cell proliferation and metabolism in the A549 human lung epithelial cells. While cytotoxicity assays revealed little difference between CR and MI exposures, proteomic and gene expression analyses unveiled both similar and unique molecular changes in A549 cells. For instance, two‐dimensional gel electrophoresis data indicated that the expression of proteins in the cell death (e.g., ALDH1A1, HTRA2 and PRDX6) and cell proliferation (e.g., FSCN1, HNRNPAB and PGK1) pathways were significantly different between the two silica particles. Reverse transcription–polymerase chain reaction data provided additional evidence supporting the proteomic findings. Preliminary assessment of the physical differences between CR and MI suggested that the extent of surface interaction between particles and cells could explain some of the observed biological effects. However, the differential dose–response curves for some other genes and proteins suggest that other physical attributes of particulate matter can also contribute to particulate matter‐related cellular toxicity. Our results demonstrated that toxicoproteomic and gene expression analyses are sensitive in distinguishing subtle toxicity differences associated with silica particles of varying physical properties compared to traditional cytotoxicity endpoints. Copyright © 2016 Her Majesty the Queen in Right of Canada. Journal of Applied Toxicology published by John Wiley & Sons, Ltd.

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“…The Akt‐signaling pathway plays an important role in the proliferation and apoptosis of RPE cells . It was reported that the activation of Akt could protect RPE cells from oxidant‐induced cell death .…”

Section: Discussionmentioning

confidence: 99%

Nobiletin protects human retinal pigment epithelial cells from hydrogen peroxide–induced oxidative damage

Liu

2018

J Biochem & Molecular Tox

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Nobiletin (3',4',5,6,7,8-hexamethoxyflavone), a dietary polymethoxylated flavonoid found in Citrus fruits, has been reported to have antioxidant effect. However, the effect of nobiletin on human retinal pigment epithelium (RPE) cells induced by hydrogen peroxide (H O ) is still unclear. Therefore, we investigated the protective effect of nobiletin against H O -induced cell death in RPE cells. Our results demonstrated that nobiletin significantly increased cell viability from oxidative stress. Nobiletin inhibited H O -induced ROS production and caspase-3/7 activity in ARPE-19 cells. Furthermore, nobiletin significantly increased Akt phosphorylation in ARPE-19 cells exposed to H O . Meanwhile, LY294002, an inhibitor of PI3K/Akt, abolished the protective effect of nobiletin against H O -induced decreased cell viability and increased caspase-3/7 activity in ARPE-19 cells. In summary, these data show that nobiletin protects RPE cells against oxidative stress through activation of the Akt-signaling pathway. Thus, nobiletin should be an oxidant that attenuates the development of age-related macular degeneration.

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PRDX6 Protects ARPE-19 Cells from Oxidative Damage via PI3K/AKT Signaling

Cited by 44 publications

References 40 publications

The role of sodium hydrosulfide in attenuating the aging process via PI3K/AKT and CaMKKβ/AMPK pathways

The role of sodium hydrosulfide in attenuating the aging process via PI3K/AKT and CaMKKβ/AMPK pathways

Responses of A549 human lung epithelial cells to cristobalite and α-quartz exposures assessed by toxicoproteomics and gene expression analysis

Nobiletin protects human retinal pigment epithelial cells from hydrogen peroxide–induced oxidative damage

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