Dexamethasone protects airway epithelial cell line NCI-H292 against lipopolysaccharide induced endoplasmic reticulum stress and apoptosis.
- Author:
Yan SHANG
1
;
Fang WANG
;
Chong BAI
;
Yi HUANG
;
Li-Jun ZHAO
;
Xiao-Peng YAO
;
Qiang LI
;
Shu-Han SUN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; drug effects; genetics; Caspase 3; metabolism; Cell Line, Tumor; Dexamethasone; pharmacology; Endoplasmic Reticulum; drug effects; metabolism; Erythromycin; pharmacology; Humans; Lipopolysaccharides; pharmacology; Mice; Mucin 5AC; genetics; metabolism; RNA, Small Interfering
- From: Chinese Medical Journal 2011;124(1):38-44
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDEndoplasmic reticulum (ER) stress and ER stress-mediated apoptosis were reported to be involved in the pathogenesis of several diseases. In a recent study, it was reported that the ER stress pathway was activated in the lungs of lipopolysaccharide (LPS)-treated mice. It was also found that the C/EBP homologous protein (CHOP), an apoptosis-related molecule, played a key role in LPS-induced lung damage. The aim of this study was to verify whether LPS could activate the ER stress response in airway epithelial cells and which molecule was involved in the pathway. This study was also aimed at finding new reagents to protect the airway epithelial cells during LPS injury.
METHODSER stress markers were observed in LPS-incubated NCI-H292 cells. SiRNA-MUC5AC was transfected into NCI-H292 cells. The effects of dexamethasone and erythromycin were observed in LPS-induced NCI-H292 cells.
RESULTSLPS incubation increased the expression of ER stress markers at the protein and mRNA levels. The knockout of MUC5AC in cells attenuated the increase in ER stress markers after incubation with LPS. Dexamethasone and erythromycin decreased caspase-3 activity in LPS-induced NCI-H292 cells.
CONCLUSIONSLPS may activate ER stress through the overexpression of MUC5AC. Dexamethasone may protect human airway epithelial cells against ER stress-related apoptosis by attenuating the overload of MUC5AC.
