Complement regulatory protein CD46 induces autophagy against oxidative stress-mediated apoptosis in normal and asthmatic airway epithelium

doi:10.1038/s41598-018-31317-5

中山醫學大學機構典藏 CSMUIR > 醫學院 > 醫學系 > 期刊論文 > Item 310902500/21024

jsp.display-item.identifier=請使用永久網址來引用或連結此文件: https://ir.csmu.edu.tw:8080/ir/handle/310902500/21024

题名:	Complement regulatory protein CD46 induces autophagy against oxidative stress-mediated apoptosis in normal and asthmatic airway epithelium
作者:	Yi-Giien Tsai;Yung-Sung Wen;Jiu-Yao Wang;Kuender D. Yang;Hai-Lun Sun;Jia-Hung Liou;Ching-Yuang Lin
贡献者:	醫學系
日期:	2018-08-28
上传时间:	2020-08-10T02:40:46Z (UTC)
出版者:	Scientific Reports
摘要:	Abstract Autophagy plays a major role in defending against oxidative stress in respiratory epithelial cells. The complement regulatory protein CD46 can enhance autophagy and decrease local complement activation at sites of inflammation. This study investigated the mechanism by which CD46 protects against oxidative stress-mediated apoptosis in respiratory epithelium in asthmatic patients. Nasal mucosa samples were obtained from 60 adults with mild asthma who received turbinectomy and 30 controls. A decreased expression of CD46 and increased apoptosis were noted in the damaged nasal epithelium from the asthmatic patients. Primary epithelial cells cultured with Dermatophagoides pteronyssinus 2 showed decreased CD46 and increased cleaved CASPASE-3A expressions. Crosslinking CD46 mAb could induce the formation of autophagosomes and LC3-II expression in primary epithelial cells. CD46 engagement could induce autophagy against hydrogen peroxide-induced epithelial cell death, whereas the autophagy inhibitor 3-methyladenine decreased this effect. In addition, CD46 engagement decreased the expressions of PRO-IL-1β and NLRP3, enhanced the expression of scaffold protein GOPC, and diminished hydrogen peroxide-induced 8-OHdG, IL-1β and IL-6 production. Silencing ATG5 in human lung epithelial A549 cells decreased CD46-activated autophagy with LC3-II. CD46 induced autophagy and decreased the oxidative stress-mediated apoptosis of respiratory epithelium, and this may offer a new therapeutic strategy to treat asthma.
URI:	https://ir.csmu.edu.tw:8080/ir/handle/310902500/21024
關聯:	Scientific Reports volume 8, Article number: 12973 (2018)
显示于类别:	[醫學系] 期刊論文

文件中的档案:

档案	描述	大小	格式	浏览次数
1-4.pdf		1915Kb	Adobe PDF	249	检视/开启

检视Licence

在CSMUIR中所有的数据项都受到原著作权保护.

TAIR相关文章

数据加载中.....