Hypoxia-Induced Activation of JAK/STAT3 Signaling Pathway Promotes Trophoblast Cell Viability and Angiogenesis in Preeclampsia

缺氧诱导的JAK/STAT3信号通路激活促进先兆子痫滋养层细胞存活和血管生成

阅读:1

Abstract

BACKGROUND To explore the effect of hypoxic preconditioning on the JAK/STAT3 signaling pathway and its effect on trophoblast cell viability and angiogenesis in preeclampsia (PE). MATERIAL AND METHODS Placental tissues from normal pregnant women and PE patients were collected to detect the expression levels of JAK and STAT3. Trophoblast cells separated from the PE patients were assigned to 4 groups. The expression levels of phosphorylated p-JAK and p-STAT3 were measured by Western blot. Cell viability, colony-forming ability, and cell apoptosis were assessed. The levels of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and hepatocyte growth factor (HGF) were determined by enzyme-linked immunosorbent assay (ELISA). RESULTS The expression levels of JAK and STAT3 were higher in the placental tissues of PE patients than in those of normal pregnant women. Compared with the blank group, in the hypoxia group the expression levels of p-JAK and p-STAT3 were increased, cell viability was promoted, the number of colonies was increased, cell apoptosis was inhibited, and the levels of VEGF, bFGF, and HGF were all elevated. However, in comparison with the hypoxia group, the expression levels of p-JAK and p-STAT3 were reduced, the cell viability was inhibited, the colonies were decreased, the levels of VEGF, bFGF, and HGF were all decreased, and cell apoptosis was promoted in the hypoxia + si-JAK group. CONCLUSIONS These findings indicate that hypoxic preconditioning may contribute to activation of the JAK/STAT3 signaling pathway, thus promoting trophoblast cell viability and angiogenesis in PE.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。