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

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.

journal_name

Med Sci Monit

journal_title

Medical science monitor : international medical journal of experimental and clinical research

authors

Xu C,Li X,Guo P,Wang J

doi

10.12659/msm.905418

subject

Has Abstract

pub_date

2017-10-14 00:00:00

pages

4909-4917

eissn

1234-1010

issn

1643-3750

pii

905418

journal_volume

23

pub_type

杂志文章

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