Toxicological effects of urban particulate matter on corneal and conjunctival epithelial cells
Toxicological Research, ISSN: 2234-2753, Vol: 36, Issue: 4, Page: 311-318
2020
- 13Citations
- 8Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations13
- Citation Indexes13
- 13
- CrossRef8
- Captures8
- Readers8
Article Description
Exposure to urban particulate matter (UPM) is a high-risk factor for various ocular surface diseases, including dry eye syndrome. However, the effects of UPM on corneal and conjunctival epithelium damage have not been fully elucidated. In this study, we investigated the toxicological effects of UPM exposure at high concentrations by using in vitro cultures. The cell viability, mucin expression, and the secreted inflammatory mediators of corneal and conjunctival epithelial cells was observed at 24 h after exposure to UPM. The progression of cell cycle was also examined by flow cytometry at 24 h after exposure to UPM. UPM reduced cell viability in a dose-dependent manner and increased cell population in S and G2 phase. The expression of mucin-1 was attenuated by UPM exposure, but that of mucin-4 was not. UPM increased interleukin (IL)-6 release and decreased IL-8 release. The intensity of 2′,7′-dichlorofluorescein diacetate (DCF-DA) was highest at 4 h of UPM exposure. In conclusion, these results suggest that UPM causes the disruption of corneal and conjunctival epithelium by decreasing cell viability, altering cell cycle, disrupting mucin, and regulating inflammatory mediators.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85079629900&origin=inward; http://dx.doi.org/10.1007/s43188-019-00034-0; http://www.ncbi.nlm.nih.gov/pubmed/33005590; https://link.springer.com/10.1007/s43188-019-00034-0; https://dx.doi.org/10.1007/s43188-019-00034-0; https://link.springer.com/article/10.1007/s43188-019-00034-0
Springer Science and Business Media LLC
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