Mesenchymal stem cells in combination with erythropoietin repair hyperoxia-induced alveoli dysplasia injury in neonatal mice via inhibition of TGF-β1 signaling

被引:31
|
作者
Luan, Yun [1 ]
Zhang, Luan [2 ]
Chao, Sun [1 ]
Liu, Xiaoli [3 ]
Li, Kaili [1 ]
Wang, Yibiao [2 ]
Zhang, Zhaohua [2 ]
机构
[1] Shandong Univ, Hosp 2, Cent Res Lab, Jinan, Peoples R China
[2] Shandong Univ, Hosp 2, Dept Pediat, Jinan, Peoples R China
[3] Shandong Univ, Hosp 2, Dept Hematol, Jinan, Peoples R China
基金
中国国家自然科学基金;
关键词
BPD; MSCs; EPO; TGF-beta; 1; ETM; ENDOTHELIAL PROGENITOR CELLS; BONE-MARROW; BRONCHOPULMONARY DYSPLASIA; TRANSFORMING GROWTH-FACTOR-BETA-1; CONDITIONAL OVEREXPRESSION; LUNG INFLAMMATION; STROMAL CELLS; TGF-BETA; TRANSITION; GROWTH;
D O I
10.18632/oncotarget.9314
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The aim of the present study is to investigate the protection effects of bone marrow mesenchymal stem cells (MSCs) in combination with EPO against hyperoxiainduced bronchopulmonary dysplasia (BPD) injury in neonatal mice. BPD model was prepared by continuous high oxygen exposure, 1x10(6) bone marrow MSCs and 5000U/kg recombinant human erythropoietin (EPO) were injected respectively. Results showed that administration of MSCs, EPO especially MSCs+ EPO significant attenuated hyperoxia-induced lung damage with a decrease of fibrosis, radical alveolar counts and inhibition of the occurrence of epithelial-mesenchymal transition (EMT). Furthermore, MSCs+ EPO co-treatment more significantly suppressed the levels of transforming growth factor-beta 1(TGF-beta 1) than MSCs or EPO alone. Collectively, these results suggested that MSCs, EPO in particular MSCs+ EPO co-treatment could promote lung repair in hyperoxia-induced alveoli dysplasia injury via inhibition of TGF-beta 1 signaling pathway to further suppress EMT process and may be a promising therapeutic strategy.
引用
收藏
页码:47082 / 47094
页数:13
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