Li Fang, Qu Huan, Cao Heng-Chang, Li Mei-Hong, Chen Chen, Chen Xiao-Fan, Yu Bo, Yu Lin, Zheng Le-Min, Zhang Wei
Biomedical Research Institute, Shenzhen Peking University-the Hong Kong University of Science and Technology Medical Center, Shenzhen, Guangdong, China.
Department of Cardiovascularology, Peking University Shenzhen Hospital, Shenzhen, Guangdong, China.
Cell Biol Int. 2015 Oct;39(10):1131-7. doi: 10.1002/cbin.10486. Epub 2015 Jun 19.
Hepatocyte growth factor (HGF) was identified as an endogenous tissue protective agent against apoptosis in many cell types. The mechanism by which HGF protects primary endothelial cells (ECs) has not yet been completely elucidated. FOXO1 and FOXO3a, two members of the FOXO family, are the most abundant FOXO isoforms in mature endothelial cells. In this study, we aimed to explore whether FOXO1 and FOXO3a play similar roles in HGF-mediated protection against apoptosis in mature endothelial cells. Our result showed that HGF prevented ECs from oxidative-stress induced apoptosis in part by inducing the phosphorylation of FOXO proteins. FOXO1 and FOXO3a are equally important in this process by regulating the expression of Bim, PUMA, FasL, and TRAIL.
肝细胞生长因子（HGF）被确定为一种内源性组织保护剂，可防止多种细胞类型发生凋亡。HGF保护原代内皮细胞（ECs）的机制尚未完全阐明。FOXO家族的两个成员FOXO1和FOXO3a是成熟内皮细胞中最丰富的FOXO亚型。在本研究中，我们旨在探讨FOXO1和FOXO3a在HGF介导的成熟内皮细胞抗凋亡保护中是否发挥相似作用。我们的结果表明，HGF部分通过诱导FOXO蛋白的磷酸化来防止ECs因氧化应激诱导的凋亡。在这个过程中，FOXO1和FOXO3a通过调节Bim、PUMA、FasL和TRAIL的表达同样重要。
