CIRCULATING EXOSOMES FROM LIPOPOLYSACCHARIDE-INDUCED ARDS MICE TRIGGER ENDOPLASMIC RETICULUM STRESS IN LUNG TISSUE
CIRCULATING EXOSOMES FROM LIPOPOLYSACCHARIDE-INDUCED ARDS MICE TRIGGER ENDOPLASMIC RETICULUM STRESS IN LUNG TISSUE
复制标题
来自脂多糖诱导的 ARDS 小鼠的循环外泌体触发肺组织中的内质网应激
DOI：
10.1097/shk.0000000000001397
复制
发表时间：
2020-07-01
期刊：
影响因子：
3.1
通讯作者：
Wang, Daoxin
中科院分区：
文献类型：
--
作者：
Tang, Xumao;Yu, Qian;Wang, Daoxin
Background: Acute respiratory distress syndrome (ARDS) is a critical clinical syndrome with high mortality rate, and few effective therapies have been found in the past 50 years, indicating that the pathogenesis of ARDS remains unclear. Exosomes, a novel cross-communication mechanism, are involved in critical diseases. However, the role of circulating exosomes in the development of ARDS remains poorly understood.Methods: In the present study, naive mice were treated with circulating exosomes from lipopolysaccharide (LPS)-induced ARDS mice or exosome-depleted serum. Histological lung damage, bronchoalveolar lavage fluid (BALF), and endoplasmic reticulum (ER) stress were measured.Results: Increased tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, total cell counts, polymorphonuclear (PMN) leukocyte proportions and myeloperoxidase (MPO) activity in BALF, and increased wet/dry weight ratios and protein concentrations in BALF were found in mice after exosome injection but not in mice treated with exosome-depleted serum. Furthermore, western blot analysis showed that circulating exosomes from ARDS mice upregulated glucose-regulated protein 78 (GRP78) and C/EBP homologous protein (CHOP) expression and downregulated beta-Catenin and VE-cadherin expression in lung tissues.Conclusions: Collectively, these data demonstrate that circulating exosomes from LPS-induced ARDS mice trigger ER stress in lung tissue, facilitating the development of ARDS, at least partly by promoting endothelial dysfunction.
