Disruption of retinal pigment epithelial cell properties under the exposure of cotinine

Abstract Cigarette smoking is a major risk factor for age-related macular degeneration (AMD), in which progressive retinal pigment epithelial (RPE) cell degeneration is a major pathological change. Nicotine is a major biologically active component in cigarette smoke. It is continuously catabolized i...

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Autores principales: Xiao-Yu Zhang, Tsz Kin Ng, Mårten Erik Brelén, Kwok Ping Chan, Di Wu, Jasmine Sum Yee Yung, Di Cao, Yumeng Wang, Shaodan Zhang, Sun On Chan, Chi Pui Pang
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Publicado: Nature Portfolio 2017
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Acceso en línea:https://doaj.org/article/436bf9f370d549f8a42d9ff98bad4762
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spelling oai:doaj.org-article:436bf9f370d549f8a42d9ff98bad47622021-12-02T11:52:30ZDisruption of retinal pigment epithelial cell properties under the exposure of cotinine10.1038/s41598-017-03283-x2045-2322https://doaj.org/article/436bf9f370d549f8a42d9ff98bad47622017-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-03283-xhttps://doaj.org/toc/2045-2322Abstract Cigarette smoking is a major risk factor for age-related macular degeneration (AMD), in which progressive retinal pigment epithelial (RPE) cell degeneration is a major pathological change. Nicotine is a major biologically active component in cigarette smoke. It is continuously catabolized into cotinine, which has longer half-life and higher concentration in tissue cells and fluids. Here we hypothesized that continuous exposure of cotinine has more potent effects on human RPE cell properties than nicotine. Human RPE cell line (ARPE-19) was treated continuously with 1–2 µM of nicotine and/or cotinine for 7 days. RPE cells treated with 2 μM cotinine and nicotine-cotinine mixture has lower MTT signals without significant changes in cell apoptosis or integrity. Moreover, RPE cell migration was retarded under cotinine treatments, but not nicotine. Both nicotine and cotinine treatments attenuated the phagocytotic activity of RPE cells. In addition, cotinine and nicotine-cotinine mixture suppressed VEGF and IL-8 expression and upregulated TIMP-2 expression. Expressions of autophagy genes were upregulated by the cotinine treatment, whereas expressions of epithelial-to-mesenchymal transition markers were downregulated. In conclusion, our study, for the first time, demonstrated that cotinine, rather than nicotine, affects the properties of RPE cells in vitro, which could explain the smoking-induced RPE pathology.Xiao-Yu ZhangTsz Kin NgMårten Erik BrelénKwok Ping ChanDi WuJasmine Sum Yee YungDi CaoYumeng WangShaodan ZhangSun On ChanChi Pui PangNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-11 (2017)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Xiao-Yu Zhang
Tsz Kin Ng
Mårten Erik Brelén
Kwok Ping Chan
Di Wu
Jasmine Sum Yee Yung
Di Cao
Yumeng Wang
Shaodan Zhang
Sun On Chan
Chi Pui Pang
Disruption of retinal pigment epithelial cell properties under the exposure of cotinine
description Abstract Cigarette smoking is a major risk factor for age-related macular degeneration (AMD), in which progressive retinal pigment epithelial (RPE) cell degeneration is a major pathological change. Nicotine is a major biologically active component in cigarette smoke. It is continuously catabolized into cotinine, which has longer half-life and higher concentration in tissue cells and fluids. Here we hypothesized that continuous exposure of cotinine has more potent effects on human RPE cell properties than nicotine. Human RPE cell line (ARPE-19) was treated continuously with 1–2 µM of nicotine and/or cotinine for 7 days. RPE cells treated with 2 μM cotinine and nicotine-cotinine mixture has lower MTT signals without significant changes in cell apoptosis or integrity. Moreover, RPE cell migration was retarded under cotinine treatments, but not nicotine. Both nicotine and cotinine treatments attenuated the phagocytotic activity of RPE cells. In addition, cotinine and nicotine-cotinine mixture suppressed VEGF and IL-8 expression and upregulated TIMP-2 expression. Expressions of autophagy genes were upregulated by the cotinine treatment, whereas expressions of epithelial-to-mesenchymal transition markers were downregulated. In conclusion, our study, for the first time, demonstrated that cotinine, rather than nicotine, affects the properties of RPE cells in vitro, which could explain the smoking-induced RPE pathology.
format article
author Xiao-Yu Zhang
Tsz Kin Ng
Mårten Erik Brelén
Kwok Ping Chan
Di Wu
Jasmine Sum Yee Yung
Di Cao
Yumeng Wang
Shaodan Zhang
Sun On Chan
Chi Pui Pang
author_facet Xiao-Yu Zhang
Tsz Kin Ng
Mårten Erik Brelén
Kwok Ping Chan
Di Wu
Jasmine Sum Yee Yung
Di Cao
Yumeng Wang
Shaodan Zhang
Sun On Chan
Chi Pui Pang
author_sort Xiao-Yu Zhang
title Disruption of retinal pigment epithelial cell properties under the exposure of cotinine
title_short Disruption of retinal pigment epithelial cell properties under the exposure of cotinine
title_full Disruption of retinal pigment epithelial cell properties under the exposure of cotinine
title_fullStr Disruption of retinal pigment epithelial cell properties under the exposure of cotinine
title_full_unstemmed Disruption of retinal pigment epithelial cell properties under the exposure of cotinine
title_sort disruption of retinal pigment epithelial cell properties under the exposure of cotinine
publisher Nature Portfolio
publishDate 2017
url https://doaj.org/article/436bf9f370d549f8a42d9ff98bad4762
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