Density-dependent expression of FGF-2 in response to oxidative stress in RPE cells in vitro

Wada, Mitsumasa; Gelfman, Claire M.; Matsunaga, Hiroshi; Alizadeh, Mitra; Morse, Lawrence S.; Handa, James T.; Hjelmeland, Leonard M.

doi:10.1076/ceyr.23.3.226.5467

Cited by 40 publications

(21 citation statements)

References 17 publications

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“…As with all cell lines, certain properties of ARPE-19 vary with culture conditions, and microarray analysis has shown gene expression differences between ARPE-19 and native RPE [52], [53]. Post-confluent ARPE-19 cells required more paraquat for equivalent toxicity as subconfluent cells, as reported in other studies, possibly due to density-dependent changes in mitochondrial-specific protein expression or turnover, such as mitochondrial MnSOD [54], or the formation of tight junctions in confluent cultures that allows transfer of protective factors, and/or growth arrest at confluency that reduces apoptosis susceptibility [55], [56]. However, the major findings in this study are the same for subconfluent and postconfluent cells.…”

Section: Discussionmentioning

confidence: 56%

The Wnt/β-Catenin Pathway Cross-Talks with STAT3 Signaling to Regulate Survival of Retinal Pigment Epithelium Cells

et al. 2012

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Wnt/β-catenin signaling is an essential pathway that regulates numerous cellular processes, including cell survival. The molecular mechanisms contributing to pro-survival Wnt signaling are mostly unknown. Signal transducer and activator of transcription proteins (STATs) are a well-described family of transcription factors. STAT3 induces expression of anti-apoptotic genes in many tissues and is a downstream mediator of protective growth factors and cytokines. In this study, we investigated whether pro-survival Wnt signaling is mediated by STAT3. The Wnt3a ligand activated Wnt signaling in the retinal pigment epithelium ARPE-19 cell line and significantly increased the viability of cells exposed to oxidative stress. Furthermore, Wnt3a increased STAT3 activation and nuclear translocation, as measured by an antibody against phosphorylated STAT3. Reducing STAT3 levels with siRNA eliminated Wnt3a-dependent protection from oxidative stress. Together, these data demonstrate a previously unknown link between Wnt3a-mediated activation of STAT3 and cell survival, and indicate cross-talk between two important pro-survival signaling pathways.

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Section: Discussionmentioning

confidence: 56%

The Wnt/β-Catenin Pathway Cross-Talks with STAT3 Signaling to Regulate Survival of Retinal Pigment Epithelium Cells

et al. 2012

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“…H 2 O 2 induced cytotoxicity in RPE cells appears to be affected by the density of cells in cultures [29]. To study this phenomenon, ARPE-19 cells plated in 96-well plates with densities of 10,000, 20,000 or 40,000 cells/well were subjected to H 2 O 2 treatment.…”

Section: Resultsmentioning

confidence: 99%

Oxidative stress causes ERK phosphorylation and cell death in cultured retinal pigment epithelium: Prevention of cell death by AG126 and 15-deoxy-delta 12, 14-PGJ2

Garg

Chang

2003

BMC Ophthalmol

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“…In contrast, IL-8 expression was found to be increased under 24-hour sodium iodate treatment14. Although there is no report on sodium iodate with FGF-2 and VEGF expression, there is a dose dependent increase in FGF-2 expression at non-toxic concentrations of THBP or hydrogen peroxide on ARPE-19 cells39, whereas oxidative stress would generally increase the expression of VEGF in RPE cells40. Different oxidative stress stimuli and treatment durations might result in different treatment responses.…”

Section: Discussionmentioning

confidence: 99%

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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Density-dependent expression of FGF-2 in response to oxidative stress in RPE cells in vitro

Abstract: These results suggest that care should be taken to control for cell density in similar types of in vitro experiments.

Cited by 40 publications

References 17 publications

The Wnt/β-Catenin Pathway Cross-Talks with STAT3 Signaling to Regulate Survival of Retinal Pigment Epithelium Cells

The Wnt/β-Catenin Pathway Cross-Talks with STAT3 Signaling to Regulate Survival of Retinal Pigment Epithelium Cells

Oxidative stress causes ERK phosphorylation and cell death in cultured retinal pigment epithelium: Prevention of cell death by AG126 and 15-deoxy-delta 12, 14-PGJ2

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

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