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

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 cotin...

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Autores principales: Zhang, Xiao-Yu, Ng, Tsz Kin, Brelén, Mårten Erik, Chan, Kwok Ping, Wu, Di, Yung, Jasmine Sum Yee, Cao, Di, Wang, Yumeng, Zhang, Shaodan, Chan, Sun On, Pang, Chi Pui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5466671/
https://www.ncbi.nlm.nih.gov/pubmed/28600524
http://dx.doi.org/10.1038/s41598-017-03283-x
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author Zhang, Xiao-Yu
Ng, Tsz Kin
Brelén, Mårten Erik
Chan, Kwok Ping
Wu, Di
Yung, Jasmine Sum Yee
Cao, Di
Wang, Yumeng
Zhang, Shaodan
Chan, Sun On
Pang, Chi Pui
author_facet Zhang, Xiao-Yu
Ng, Tsz Kin
Brelén, Mårten Erik
Chan, Kwok Ping
Wu, Di
Yung, Jasmine Sum Yee
Cao, Di
Wang, Yumeng
Zhang, Shaodan
Chan, Sun On
Pang, Chi Pui
author_sort Zhang, Xiao-Yu
collection PubMed
description 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.
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spelling pubmed-54666712017-06-14 Disruption of retinal pigment epithelial cell properties under the exposure of cotinine Zhang, Xiao-Yu Ng, Tsz Kin Brelén, Mårten Erik Chan, Kwok Ping Wu, Di Yung, Jasmine Sum Yee Cao, Di Wang, Yumeng Zhang, Shaodan Chan, Sun On Pang, Chi Pui Sci Rep Article 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. Nature Publishing Group UK 2017-06-09 /pmc/articles/PMC5466671/ /pubmed/28600524 http://dx.doi.org/10.1038/s41598-017-03283-x Text en © The Author(s) 2017 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Zhang, Xiao-Yu
Ng, Tsz Kin
Brelén, Mårten Erik
Chan, Kwok Ping
Wu, Di
Yung, Jasmine Sum Yee
Cao, Di
Wang, Yumeng
Zhang, Shaodan
Chan, Sun On
Pang, Chi Pui
Disruption of retinal pigment epithelial cell properties under the exposure of cotinine
title 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_short 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
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5466671/
https://www.ncbi.nlm.nih.gov/pubmed/28600524
http://dx.doi.org/10.1038/s41598-017-03283-x
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