Disruption of retinal pigment epithelial cell properties under the exposure of cotinine
Publication in refereed journal


摘要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.
著者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
期刊名稱Scientific Reports
出版社Nature Publishing Group
關鍵詞Mechanisms of disease, Risk factors

上次更新時間 2021-25-01 於 02:45