CD28 Deficiency Ameliorates Blast Exposure-Induced Lung Inflammation, Oxidative Stress, Apoptosis, and T Cell Accumulation in the Lungs via the PI3K/Akt/FoxO1 Signaling Pathway

doi:10.1155/2019/4848560

IMR OpenIR

	CD28 Deficiency Ameliorates Blast Exposure-Induced Lung Inflammation, Oxidative Stress, Apoptosis, and T Cell Accumulation in the Lungs via the PI3K/Akt/FoxO1 Signaling Pathway
	Liu, Yunen 1; Tong, Changci 1; Xu, Ying 2; Gong, Peifang 1; Liu, Ying 1; Shi, Lin 1; Shi, Xiuyun 2; Zhao, Yan 3; Bi, Guangyuan 4; Jin, Hongxu 1; Hou, Mingxiao 1
通讯作者	Bi, Guangyuan(biguangyuan18@163.com) ; Jin, Hongxu(hongxuj@126.com) ; Hou, Mingxiao(houmingxiao188@163.com)
	2019-09-02
发表期刊	OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
ISSN	1942-0900
卷号	2019 页码:15
摘要	Although CD28 is associated with the expression of inflammatory mediators, apoptosis-related protein, immunosuppression, and tumorigenesis, the effects of CD28 deficiency on blast exposure-induced lung injury have not been investigated. In this study, we have explored the effects of CD28 on blast exposure-induced lung injury and studied its potential molecular mechanisms. A mouse model of blast exposure-induced acute lung injury was established. Sixty C57BL/6 wild-type (WT) and CD28 knockout (CD28(-/-)) mice were randomly divided into control or model groups. Lung tissue samples were collected 24 h and 48 h after blast injury. Histopathological changes and the expressions of inflammatory-related proteins were detected by hematoxylin-eosin, immunohistochemistry, and immunofluorescence staining. Apoptosis and oxidative stress were evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining and reactive oxygen species (ROS). Inflammation, apoptosis, oxidative stress, and related pathway protein expression were studied by western blotting. In addition, the levels of CD3 and CD28 proteins were measured by flow cytometry. In the current study, we found that CD28 deficiency significantly inhibited blast exposure-induced increases in the lung weight/body weight ratio and wet weight/dry weight ratio; decreased the infiltration of CD44(+) leukocytes, CD163(+) macrophages, and CD3(+) T cells into the lungs; reduced the expressions of proinflammatory cytokines including IL-1 beta, TNF-alpha, and IL-6; and markedly increased IL-10 expression. CD28 deficiency also significantly attenuated blast exposure-induced ROS, MDA5, and IRE alpha expressions; increased SOD-1 expression; lowered the number of apoptotic cells and Bax, Caspase-3, and active Caspase-8 expressions; and increased Bcl-2 expression. Additionally, CD28 deficiency significantly ameliorated blast exposure-induced increases of p-PI3K and p-Akt and ameliorated the decrease in the p-FoxO1 expression. Our results suggest that CD28 deficiency has a protective effect on blast exposure-induced lung injury, which might be associated with the PI3K/Akt/FoxO1 signaling pathway.
资助者	Edanz Group China ; Liaoning Province Key Scientific and Technological Project ; PLA Foundation of China
DOI	10.1155/2019/4848560
收录类别	SCI
语种	英语
资助项目	Edanz Group China ; Liaoning Province Key Scientific and Technological Project[201602786] ; Liaoning Province Key Scientific and Technological Project[20170540947] ; PLA Foundation of China[CSY12J002] ; PLA Foundation of China[AWS14L008] ; PLA Foundation of China[CSY13J003]
WOS研究方向	Cell Biology
WOS类目	Cell Biology
WOS记录号	WOS:000486396400004
出版者	HINDAWI LTD
引用统计	被引频次：19[WOS] [WOS记录] [WOS相关记录]
文献类型	期刊论文
条目标识符	http://ir.imr.ac.cn/handle/321006/135468
专题	中国科学院金属研究所
通讯作者	Bi, Guangyuan; Jin, Hongxu; Hou, Mingxiao
作者单位	1.Dept Gen Hosp Northern Theater Command, Emergency Med, Lab Rescue Ctr Severe Trauma PLA, 83 Rd, Shenyang 110016, Liaoning, Peoples R China 2.Dept Gen Hosp Northern Theater Command, Radiat Oncol, Shenyang 110016, Liaoning, Peoples R China 3.Chinese Acad Sci, Inst Met Res, 72 Wenhua Rd, Shenyang 110016, Liaoning, Peoples R China 4.Natl Def Univ, Med Serv Dept, Joint Serv Coll, PLA 23rd,Taiping Rd, Beijing 100858, Peoples R China
推荐引用方式 GB/T 7714	Liu, Yunen,Tong, Changci,Xu, Ying,et al. CD28 Deficiency Ameliorates Blast Exposure-Induced Lung Inflammation, Oxidative Stress, Apoptosis, and T Cell Accumulation in the Lungs via the PI3K/Akt/FoxO1 Signaling Pathway[J]. OXIDATIVE MEDICINE AND CELLULAR LONGEVITY,2019,2019:15.
APA	Liu, Yunen.,Tong, Changci.,Xu, Ying.,Gong, Peifang.,Liu, Ying.,...&Hou, Mingxiao.(2019).CD28 Deficiency Ameliorates Blast Exposure-Induced Lung Inflammation, Oxidative Stress, Apoptosis, and T Cell Accumulation in the Lungs via the PI3K/Akt/FoxO1 Signaling Pathway.OXIDATIVE MEDICINE AND CELLULAR LONGEVITY,2019,15.
MLA	Liu, Yunen,et al."CD28 Deficiency Ameliorates Blast Exposure-Induced Lung Inflammation, Oxidative Stress, Apoptosis, and T Cell Accumulation in the Lungs via the PI3K/Akt/FoxO1 Signaling Pathway".OXIDATIVE MEDICINE AND CELLULAR LONGEVITY 2019(2019):15.