Continuous exposure to non-lethal doses of sodium iodate induces retinal pigment epithelial cell dysfunction
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摘要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.
著者Zhang XY, Ng TK, Brelén ME, Wu D, Wang JX, Chan KP, Yung JS, Cao D, Wang Y, Zhang S, Chan SO, Pang CP
期刊名稱Scientific Reports
出版年份2016
月份11
日期16
卷號6
出版社Springer Nature
頁次37279
國際標準期刊號2045-2322
電子國際標準期刊號2045-2322
語言美式英語

上次更新時間 2021-18-01 於 01:17