Exposure to particulate matter (PM2.5) weakens corneal defense by downregulating thrombospondin-1 and tight junction proteins

作者：Liangliang Niu, Jiamin Liu, Huan Xu, Binghui Liu, Maomao Song, Chunchun Hu, Rui Jiang, Xinghuai Sun, Yuan Lei · 发表于：Ecotoxicology and Environmental Safety · 年份：2024 · DOI：10.1016/j.ecoenv.2024.117276 · 被引用次数：10 · 研究领域：Barrier Structure and Function Studies、Air Quality and Health Impacts、Dietary Effects on Health

Fine particulate matter (PM 2.5 ) induces ocular surface toxicity through pyroptosis, oxidative stress, autophagy, and inflammatory responses. However, the precise molecular pathways through which PM 2.5 causes corneal damage remain unclear. This study aims to investigate the underlying mechanisms by exposing human corneal epithelial cells (HCECs) to PM 2.5 . After the morphology and chemical composition analysis of the PM samples, we conducted both in vivo and in vitro experiments to investigate PM 2.5 -induced corneal epithelial damage. We assessed corneal barrier function in HCECs using transepithelial electrical resistance (TEER) assays. To explore the molecular mechanisms of PM 2.5 -induced corneal epithelial damage, we performed whole-transcriptome resequencing, quantitative RT-PCR, and western blotting in vitro. In addition, we analyzed mouse corneas exposed to concentrated ambient PM 2.5 through immunofluorescence staining to observe the resulting changes in corneal epithelial protein expression in vivo. Our results showed significant impairment of corneal epithelial barrier function in PM 2.5 -treated HCECs, as indicated by decreased TEER values. The expression of thrombospondin-1 (THBS1) and claudin-1, both key factors for maintaining corneal epithelial barrier integrity, was markedly reduced at the gene and protein levels in both in vitro and in vivo PM 2.5 exposure models. Moreover, the levels of tight junction-associated proteins, including occludin, zonula occlu...