Maresin 1 Maintains the Permeability of Lung Epithelial Cells In Vitro and In Vivo

被引：17

作者：

Chen, Lin ^{[1
,2
]}

Liu, Hong ^{[1
]}

Wang, Yaxin ^{[1
,2
]}

Xia, Haifa ^{[2
,3
]}

Gong, Jie ^{[1
,2
]}

Li, Bo ^{[2
,3
]}

Yao, Shanglong ^{[2
,3
]}

Shang, You ^{[1
,2
]}

机构：

[1] Huazhong Univ Sci & Technol, Tongji Med Coll, Inst Anesthesiol & Crit Care Med, Union Hosp,Dept Crit Care Med, 1277 Jiefang Ave, Wuhan 430022, Hubei, Peoples R China

[2] Huazhong Univ Sci & Technol, Tongji Med Coll, Inst Anesthesiol & Crit Care Med, Union Hosp,Dept Anesthesiol, 1277 Jiefang Ave, Wuhan 430022, Hubei, Peoples R China

[3] Huazhong Univ Sci & Technol, Union Hosp, Dept Anesthesiol, Tongji Med Coll, 1277 Jiefang Ave, Wuhan 430022, Hubei, Peoples R China

来源：

INFLAMMATION | 2016年 / 39卷 / 06期

基金：

中国国家自然科学基金;

关键词：

Maresin; 1; lipopolysaccharide; acute lung injury; tight junction; permeability; RESPIRATORY-DISTRESS-SYNDROME; LIPOXIN RECEPTOR AGONIST; BARRIER DYSFUNCTION; LIPID MEDIATORS; TIGHT JUNCTIONS; INJURY; INFLAMMATION; RESOLUTION; CLAUDINS; EXPRESSION;

D O I：

10.1007/s10753-016-0433-0

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Previous reports showed that Maresin 1 (MaR1) possessed organ protection effects and could attenuate acute lung injury. Here, we aim to figure out whether MaR1 can maintain the permeability of lung epithelial cells by regulating the expression of tight junction protein during lung injury. Monolayer of murine lung epithelial cells was stimulated by lipopolysaccharide (LPS) with or without MaR1 and the permeability was evaluated. The expression of Claudin-1 and ZO-1 in lung epithelial cells was analyzed by immunofluorescence staining and western blotting. MaR1 was given to the mice after LPS induced acute lung injury. The permeability of lung was assessed by Evans Blue extravasation, lung wet/dry ratio and protein concentration in bronchoalveolar lavage fluid. Lung injury score was also evaluated. The expression of Claudin-1 and ZO-1 in the lung was analyzed by immunofluorescence staining. Results showed that MaR1 maintained the permeability of lung epithelial cells and upregulated the expression of Claudin-1 and ZO-1 after LPS stimulation. In acute lung injury mice, MaR1 upregulated the expression of Claudin-1 and ZO-1, decreased lung permeability, and reduced lung injury. In summary, this study suggests that MaR1 can maintain the permeability of lung epithelial cells by upregulating the expression of Claudin-1 and ZO-1 in acute lung injury.

引用

页码：1981 / 1989

页数：9

共 42 条

[1] Maresin 1 biosynthesis during platelet-neutrophil interactions is organ-protective [J].