title: Continuous exposure to non-lethal doses of sodium iodate induces retinal pigment epithelial cell dysfunction.
abstract: 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.
authors.affiliation: Department of Ophthalmology and Visual Sciences, and The Chinese University of Hong Kong, Hong Kong.|Department of Ophthalmology, The Fourth People's Hospital of Shenyang, Shenyang, China.|Shenyang Key Laboratory of Ophthalmology, Shenyang, China.
authors.forename: Xiao-Yu
authors.initials: XY
authors.lastname: Zhang
authors.affiliation: Department of Ophthalmology and Visual Sciences, and The Chinese University of Hong Kong, Hong Kong.
authors.forename: Tsz Kin
authors.initials: TK
authors.lastname: Ng
authors.affiliation: Department of Ophthalmology and Visual Sciences, and The Chinese University of Hong Kong, Hong Kong.
authors.forename: Mårten Erik
authors.initials: ME
authors.lastname: Brelén
authors.affiliation: Department of Ophthalmology, The Fourth People's Hospital of Shenyang, Shenyang, China.|Shenyang Key Laboratory of Ophthalmology, Shenyang, China.
authors.forename: Di
authors.initials: D
authors.lastname: Wu
authors.affiliation: Department of Ophthalmology and Visual Sciences, and The Chinese University of Hong Kong, Hong Kong.
authors.forename: Jian Xiong
authors.initials: JX
authors.lastname: Wang
authors.affiliation: Department of Ophthalmology and Visual Sciences, and The Chinese University of Hong Kong, Hong Kong.
authors.forename: Kwok Ping
authors.initials: KP
authors.lastname: Chan
authors.affiliation: Department of Ophthalmology and Visual Sciences, and The Chinese University of Hong Kong, Hong Kong.
authors.forename: Jasmine Sum Yee
authors.initials: JSY
authors.lastname: Yung
authors.affiliation: Department of Ophthalmology and Visual Sciences, and The Chinese University of Hong Kong, Hong Kong.
authors.forename: Di
authors.initials: D
authors.lastname: Cao
authors.affiliation: Department of Ophthalmology and Visual Sciences, and The Chinese University of Hong Kong, Hong Kong.
authors.forename: Yumeng
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Ophthalmology, The Fourth People's Hospital of Shenyang, Shenyang, China.|Shenyang Key Laboratory of Ophthalmology, Shenyang, China.
authors.forename: Shaodan
authors.initials: S
authors.lastname: Zhang
authors.affiliation: School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong.
authors.forename: Sun On
authors.initials: SO
authors.lastname: Chan
authors.affiliation: Department of Ophthalmology and Visual Sciences, and The Chinese University of Hong Kong, Hong Kong.
authors.forename: Chi Pui
authors.initials: CP
authors.lastname: Pang
mesh_terms: D002460:Cell Line; D002465:Cell Movement / Q000187:drug effects*; D004305:Dose-Response Relationship, Drug; D004847:Epithelial Cells / Q000187:drug effects* / Q000378:metabolism; D016222:Fibroblast Growth Factor 2 / Q000235:genetics / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D007452:Iodates / Q000494:pharmacology*; D008268:Macular Degeneration / Q000235:genetics / Q000378:metabolism; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D010587:Phagocytosis / Q000187:drug effects; D055213:Retinal Pigment Epithelium / Q000166:cytology*; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics / Q000378:metabolism; D062826:Zonula Occludens-1 Protein / Q000378:metabolism
chemical_list: D007452:Iodates; C502070:MAP1LC3B protein, human; D008869:Microtubule-Associated Proteins; C569042:TJP1 protein, human; D042461:Vascular Endothelial Growth Factor A; D062826:Zonula Occludens-1 Protein; D016222:Fibroblast Growth Factor 2; C032285:sodium iodate