Overexpression of bone morphogenetic protein-9 inhibits lipopolysaccharide-induced inflammatory response and apoptosis in alveolar epithelial cells
10.3969/j.issn.1000-484X.2025.11.004
- VernacularTitle:过表达骨形态发生蛋白-9抑制脂多糖诱导的肺泡上皮细胞炎症反应及凋亡
- Author:
Jiaxin WANG
1
;
Yaodi XU
;
Zhouli TAN
;
Chunyang ZHANG
;
Li XIAO
;
Xuxin CHEN
;
Zhihai HAN
Author Information
1. 解放军总医院第六医学中心呼吸与危重症医学科,北京 100048
- Publication Type:Journal Article
- Keywords:
BMP9;
Alveolar epithelial cells;
Inflammation;
Apoptosis;
Acute lung injury
- From:
Chinese Journal of Immunology
2025;41(11):2578-2582
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effect of bone morphogenetic protein-9(BMP9)overexpression on inflammatory response and apoptosis of alveolar epithelial cells induced by lipopolysaccharide(LPS).Methods:A549 cells were stimulated with 0.1 μg/ml LPS,expressions and changes of BMP9 protein at different time points(LPS stimulation for 0 h,6 h,12 h,24 h)were detected by Western blot.Expression of BMP9 in A549 cells was up-regulated by transfection of BMP9 plasmid,and the transfection efficiency was verified by Western blot and qPCR.After 12 h of LPS stimulation,levels of inflammatory factors TNF-α,IL-6,IL-1β in cell supernatant were detected by ELISA,expressions of anti-apoptotic protein(Bcl-2)and pro-apoptotic protein(Bax)were detected by Western blot,and apoptosis of cells was detected by TUNEL staining.Results:With the extension of LPS stimulation time,expression of BMP9 was down-regulated.Overexpression of BMP9 successfully up-regulated expression of BMP9 in A549 cells.LPS stimulation promoted secretions of TNF-α,IL-6 and IL-1β from A549 cells,increased apoptosis,promoted Bcl-2 expression while inhibited Bax expression.Overexpression of BMP9 inhibited TNF-α,IL-6 and IL-1β releasing,decreased apoptosis,inhibited Bcl-2 expression,while promoted Bax expression.Conclusion:In LPS-stimulated A549 cells,BMP9 expression is gradually decreased at a time-depen-dent manner.Overexpression of BMP9 can inhibit LPS-induced inflammatory response and apoptosis in A549 cells.
