Airborne fine particulate matter (PM2.5) damages the inner blood-retinal barrier by inducing inflammation and ferroptosis in retinal vascular endothelial cells

被引：27

作者：

Gu, Yuzhou ^{[1
]}

Hao, Shengjie ^{[1
]}

Liu, Kaiyuan ^{[2
]}

Gao, Mengqin ^{[2
]}

Lu, Bing ^{[1
]}

Sheng, Feiyin ^{[1
]}

Zhang, Li ^{[1
]}

Xu, Yili ^{[1
]}

Wu, Di ^{[1
]}

Han, Yu ^{[1
]}

Chen, Shuying ^{[1
]}

Zhao, Wei ^{[1
]}

Lou, Xiaoming ^{[3
]}

Wang, Xiaofeng ^{[3
]}

Li, Peng ^{[2
]}

Chen, Zhijian ^{[3
]}

Yao, Ke ^{[1
]}

Fu, Qiuli ^{[1
]}

机构：

[1] Zhejiang Univ, Eye Ctr, Affiliated Hosp 2, Sch Med,Zhejiang Prov Key Lab Ophthamol, Hangzhou, Zhejiang, Peoples R China

[2] Zhejiang Univ, Coll Opt Sci & Engn, State Key Lab Modern Opt Instrumentat, Hangzhou 310027, Zhejiang, Peoples R China

[3] Zhejiang Prov Ctr Dis Control & Prevent, Dept Environm & Ocapat Hlth, Hangzhou 310051, Zhejiang, Peoples R China

来源：

SCIENCE OF THE TOTAL ENVIRONMENT | 2022年 / 838卷

基金：

中国国家自然科学基金;

关键词：

PM2.5; Ferroptosis; Inflammation; Inner blood-retinal barrier; Retina; AIR-POLLUTION; LIPID-PEROXIDATION; TRIGGERS AUTOPHAGY; OUTPATIENT VISITS; DEATH; INTENSITY; CONJUNCTIVITIS; DECORRELATION; BREAKDOWN; FAILURE;

D O I：

10.1016/j.scitotenv.2022.156563

中图分类号：

X [环境科学、安全科学];

学科分类号：

08 ; 0830 ;

摘要：

This study was the first to explore the effect of airborne fine particulate matter (PM2.5) exposure on the inner blood-retinal barrier (iBRB). In this study, retinal vascular permeability and diameter were enhanced in the PM2.5-exposed animal model (1 mg/mL PM2.5, 10 mu L per eye, 4 times per day, 3 days), together with observable retinal edema and increased inflammation level in retina. PM2.5-induced cell damage in human retinal microvascular endothelial cells (HRMECs) occurred in a time- and dose-dependent manner. Decreased cell viability, proliferation, migration, and angiogenesis, as well as increased apoptosis and inflammation, were observed. Iron overload and excessive lipid oxidation were also discovered after PM2.5 exposure (25, 50, and 100 mu g/mL PM2.5 for 24 h), along with significantly altered expression of ferroptosis-related genes, such as prostaglandin-endoperoxide synthase 2, glutathione peroxidase 4, and ferritin heavy chain 1. Moreover, Ferrostatin-1, an inhibitor of ferroptosis, evidently alleviated the PM2.5-induced cytotoxicity of HRMECs. The present study investigated the in vivo effects of PM2.5 on retinas, revealing that PM2.5 exposure induced retinal inflammation, vascular dilatation, and caused damage to the iBRB. The crucial role of ferroptosis was discovered during PM2.5-induced HRMEC cytotoxicity and dysfunction, indicating a potential precautionary target in air pollution-associated retinal vascular diseases.

引用

页数：14

共 76 条

[1] Deferoxamine Treatment Prevents Post-Stroke Vasoregression and Neurovascular Unit Remodeling Leading to Improved Functional Outcomes in Type 2 Male Diabetic Rats: Role of Endothelial Ferroptosis [J].