bFGF overexpression adipose derived mesenchymal stem cells improved the survival of pulmonary arterial endothelial cells via PI3k/Akt signaling pathway

被引:14
作者
Wang, Pengbo [1 ,2 ]
Li, Jun [1 ]
Zhang, Caixin [1 ,2 ]
Luo, Lin [2 ]
Ni, Songshi [1 ]
Tang, Zhiyuan [1 ]
机构
[1] Nantong Univ, Affiliated Hosp, Dept Resp & Crit Care Med, Nantong 226001, Jiangsu, Peoples R China
[2] Nantong Univ, Med Sch, Nantong, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
bFGF; ASC; HPAEC; PI3k/Akt; PAH; PLEXIFORM LESIONS; GROWTH; PROLIFERATION; TISSUE; DIFFERENTIATION; HYPERTENSION; MIGRATION; PROMOTES;
D O I
10.1016/j.biocel.2019.06.004
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Pulmonary arterial hypertension (PAH) is characterized as pulmonary arterial endothelial dysfunction and endothelial cells over proliferation, therefore, the repair of pulmonary arterial endothelial cells has been a common goal in treating PAH. In the present study, human adipose derived mesenchymal stem cells (ASCs) were transfected with bFGF lentiviral vector and co-cultured with monocrotaline pyrrole treated human pulmonary arterial endothelial cells (HPAECs). The results showed that bFGF-ASCs improved the proliferation, viability and decreased the apoptosis of HPAECs, besides, improved PAH was observed in PAH rat models. Western blot analysis showed that the PI3k and p-Akt protein expression level increased in HPAECs, suggesting the activation of the PI3k/Akt signaling pathway. With the administration of LY294002, the bFGF induced HPAECs survival and PI3k/Akt signaling activation were successfully blocked. The present study demonstrated that bFGF transfected ASCs improved the survival of HPAECs by activating the PI3k/Akt pathway.
引用
收藏
页码:87 / 94
页数:8
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