Malondialdehyde induces autophagy dysfunction and VEGF secretion in the retinal pigment epithelium in age-related macular degeneration

Ye, Fuxiang; Kaneko, Hiroki; Hayashi, Yoshinori; Takayama, Kei; Hwang, Shiang-Jyi; Nishizawa, Yuji; Kimoto, Reona; Nagasaka, Yosuke; Tsunekawa, Taku; Matsuura, Tamifusa; Yasukawa, Tsutomu; Kondo, Takaaki; Terasaki, Hiroko

doi:10.1016/j.freeradbiomed.2016.02.027

Cited by 52 publications

(58 citation statements)

References 70 publications

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“…Similarly, 1 and 3-day hydrogen peroxide treatments also increase the autophagic activity in ARPE-19 cells, but reduces in the 14-day treatment19. Increase in autophagic activity has been shown to be associated with the AMD pathology43637. Moreover, the upregulation in autophagy pathway could also be associated with the reduced RPE cell viability (Fig.…”

Section: Discussionmentioning

confidence: 72%

Continuous exposure to non-lethal doses of sodium iodate induces retinal pigment epithelial cell dysfunction

Zhang

Brelén

et al. 2016

Sci Rep

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Age-related macular degeneration (AMD), characterized by progressive degeneration of retinal pigment epithelium (RPE), is the major cause of irreversible blindness and visual impairment in elderly population. We previously established a RPE degeneration model using an acute high dose sodium iodate to induce oxidative stress. Here we report findings on a prolonged treatment of low doses of sodium iodate on human RPE cells (ARPE-19). RPE cells were treated continuously with low doses (2–10 mM) of sodium iodate for 5 days. Low doses (2–5 mM) of sodium iodate did not reduce RPE cell viability, which is contrasting to cell apoptosis in 10 mM treatment. These low doses are sufficient to retard RPE cell migration and reduced expression of cell junction protein ZO-1. Phagocytotic activity of RPE cells was attenuated by sodium iodate dose-dependently. Sodium iodate also increased expression of FGF-2, but suppressed expression of IL-8, PDGF, TIMP-2 and VEGF. Furthermore, HTRA1 and epithelial-to-mesenchymal transition marker proteins were downregulated, whereas PERK and LC3B-II proteins were upregulated after sodium iodate treatment. These results suggested that prolonged exposure to non-lethal doses of oxidative stress induces RPE cell dysfunctions that resemble conditions in AMD. This model can be used for future drug/treatment investigation on AMD.

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Section: Discussionmentioning

confidence: 72%

Continuous exposure to non-lethal doses of sodium iodate induces retinal pigment epithelial cell dysfunction

Zhang

Brelén

et al. 2016

Sci Rep

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“…Among the ocular diseases, there has been an accumulation of evidence demonstrating a significant relationship between oxidative stress and AMD, both in vitro and in vivo [10,29,30]. We previously demonstrated that MDA, an oxidative stress marker, is not only a marker of AMD, but is also a direct contributor to the pathogenesis of AMD [31]. In particular, we showed that serum MDA levels in patients with nAMD were significantly higher than in control subjects, and that there was a significant correlation between serum MDA levels and CNV area [12].…”

Section: Discussionmentioning

confidence: 99%

Diacron reactive oxygen metabolites and biological antioxidant potential tests for patients with age-related macular degeneration

et al. 2020

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Background: Previously, we showed that serum malondialdehyde (MDA) was significantly higher in patients with neovascular age-related macular degeneration (nAMD) than in those without AMD. The Diacron reactive oxygen metabolites (d-ROMs) and biological antioxidant potential (BAP) tests are known markers of oxidative stress. The aim of this study was to use d-ROMs and BAP tests to evaluate changes in systemic oxidative stress in patients with nAMD. Methods: Blood serum samples were collected from 34 patients with nAMD (mean age: 76.5 ± 7.7 years; 22 men) and 20 control subjects (mean age: 62.9 ± 14.0 years; 10 men), and d-ROMs and BAP tests were examined.Results: In men, the mean level of d-ROMs for the nAMD patients was significantly higher than that for the controls (312.0 ± 52.4 vs. 275.1 ± 45.5 U.CARR, respectively; P < .05). There was a significant correlation between d-ROM level and CNV lesion area in the male nAMD group (r = .42, P = .05). There were no significant differences in mean BAP test results between the nAMD patients and controls for either sex (men: 2241 ± 549 vs. 2136 ± 246 μmol/L; women: 2263 ± 292 vs. 2335 ± 161 μmol/L). Conclusion:The d-ROMs test may provide a useful indicator of nAMD in men but not in women.

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“…24 ROS cause cell damage directly but can also trigger intracellular signal transduction that leads to various outcomes in different cell types involved in AMD. 25 Hartnett et al demonstrated that in CECs, overexpressing active Rap1a by 8CPT inhibits TNF-α-induced CEC migration by inhibiting NADPH oxidase-dependent NF-kB and Rac1 activation. This result suggests that Rap1a de-escalates CNV development by interfering with ROSdependent signaling.…”

Section: Discussionmentioning

confidence: 99%

Activation of the Small GTPase Rap1 Inhibits Choroidal Neovascularization by Regulating Cell Junctions and ROS Generation in Rats

Zhang

Wang

et al. 2018

Current Eye Research

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Malondialdehyde induces autophagy dysfunction and VEGF secretion in the retinal pigment epithelium in age-related macular degeneration

Cited by 52 publications

References 70 publications

Continuous exposure to non-lethal doses of sodium iodate induces retinal pigment epithelial cell dysfunction

Continuous exposure to non-lethal doses of sodium iodate induces retinal pigment epithelial cell dysfunction

Diacron reactive oxygen metabolites and biological antioxidant potential tests for patients with age-related macular degeneration

Activation of the Small GTPase Rap1 Inhibits Choroidal Neovascularization by Regulating Cell Junctions and ROS Generation in Rats

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