Abstract：
Atmospheric pollution has been demonstrated to be associated with ocular surface diseases characterized by corneal epithelial damage, including impaired barrier function and squamous metaplasia. However, the specific mechanisms underlying the impact of atmospheric pollution on corneal damage are still unknow. To address this gap in knowledge, we conducted a study using a whole-body exposure system to investigate the detrimental effects of traffic-related air pollution, specifically diesel exhaust (DE), on corneal epithelium in C57BL/6 mice over a 28-day period. Following DE exposure, the pathological alterations in corneal epithelium, including significant increase in corneal thickness and epithelial stratification, were observed in mice. Additionally, exposure to DE was also shown to disrupt the barrier functions of corneal epithelium, leading to excessive proliferation of basal cells and even causing squamous metaplasia in corneal epithelium. Further studies have found that the activation of yes-associated protein (YAP), characterized by nuclear translocation, may play a significant role in DE-induced corneal squamous metaplasia. In vitro assays confirmed that DE exposure triggered the YAP/β-catenin pathway, resulting in squamous metaplasia and destruction of barrier functions. These findings provide the preliminary evidence that YAP activation is one of the mechanisms of the damage to corneal epithelium caused by traffic-related air pollution. These findings contribute to the knowledge base for promoting eye health in the context of atmospheric pollution.
摘要：
大气污染已被证明与以角膜上皮损伤为特征的眼表疾病有关，包括屏障功能受损和鳞状上皮化生。然而,大气污染对角膜损伤影响的具体机制尚不清楚。为了解决这个知识差距，我们使用全身暴露系统进行了一项研究，以调查与交通有关的空气污染的有害影响，特别是柴油机排气(DE)，在28天的时间内，C57BL/6小鼠的角膜上皮上。DE暴露后，角膜上皮的病理改变，包括角膜厚度和上皮分层的显着增加，在小鼠中观察到。此外,暴露于DE也被证明会破坏角膜上皮的屏障功能，导致基底细胞过度增殖，甚至导致角膜上皮鳞状上皮化生。进一步的研究发现，Yes相关蛋白（YAP）的激活，以核易位为特征，可能在DE诱导的角膜鳞状上皮化生中起重要作用。体外试验证实，DE暴露触发了YAP/β-catenin途径，导致鳞状上皮化生和屏障功能的破坏。这些发现提供了初步证据，表明YAP激活是交通相关空气污染引起的角膜上皮损伤的机制之一。这些发现有助于在大气污染背景下促进眼睛健康的知识库。
