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实际环境 PM 通过 Wnt/β-连环蛋白信号诱导角膜上皮屏障破坏。

Real-ambient PM induced corneal epithelial barrier disruption through Wnt/β-catenin signaling.

机构信息

Department of Occupational and Environmental Health, School of Public Health, Qingdao University, Qingdao 266071, China.

Department of Occupational and Environmental Health, School of Public Health, Qingdao University, Qingdao 266071, China; Affiliated Hospital of Qingdao University and Biomedical Sciences Institute of Qingdao University (Qingdao Branch of SJTU Bio-X Institutes), Qingdao University, Qingdao, Shandong 266003, China.

出版信息

Ecotoxicol Environ Saf. 2024 Nov 1;286:117197. doi: 10.1016/j.ecoenv.2024.117197. Epub 2024 Oct 22.

Abstract

Continued daily exposure to fine particulate matter (PM) is linked to increasing risks of ocular surface diseases. However, further study is needed to understand how real-ambient PM disrupts the barrier function of the corneal epithelial layers and its underlying mechanism. In our study, we utilized a real-ambient PM exposure system to investigate its effects on the corneal epithelial barrier in C57BL/6Jmice over 4 and 8 weeks. The mean concentration of PM in the exposure chambers over 8 weeks was 140.18 μg/m. Following 4 and 8 weeks of continuous PM exposure, we observed disorganized cellular arrangements in the corneal epithelium of mice. Moreover, PM exposure led to a significant loss of microvilli on the surface of corneal epithelial cells and noticeable disconnections among epithelial cell layers. Subsequent in vitro analysis revealed that 100 μg/mL PM activated the Wnt/β-catenin signaling pathway in corneal epithelium, resulting in decreased expression 1.81 fold and 2.25 fold of E-cadherin and ZO-1, respectively, ultimately impairing the corneal epithelial barrier function. Our findings provide the knowledge base for promoting eye health in the context of atmospheric pollution.

摘要

持续的日常细颗粒物(PM)暴露与眼部表面疾病风险的增加有关。然而,仍需要进一步的研究来了解真实环境 PM 如何破坏角膜上皮层的屏障功能及其潜在机制。在我们的研究中,我们利用真实环境 PM 暴露系统在 4 周和 8 周内研究了其对 C57BL/6J 小鼠角膜上皮屏障的影响。暴露室内 PM 的平均浓度在 8 周内达到 140.18μg/m³。在持续 4 周和 8 周的 PM 暴露后,我们观察到小鼠角膜上皮细胞的细胞排列紊乱。此外,PM 暴露导致角膜上皮细胞表面微绒毛明显丢失,上皮细胞层之间出现明显的连接中断。随后的体外分析表明,100μg/mL PM 激活了角膜上皮细胞中的 Wnt/β-catenin 信号通路,导致 E-cadherin 和 ZO-1 的表达分别降低了 1.81 倍和 2.25 倍,最终损害了角膜上皮屏障功能。我们的发现为大气污染背景下促进眼部健康提供了知识基础。

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