Decreased Cyr61 under Hypoxia Induces Extravillous Trophoblasts Apoptosis and Preeclampsia

During placental development, oxygen environment is not only critical for trophoblasts migration and invasion, but also fundamental for appropriate placental perfusion. Cysteine-rich 61 （Cyr61, CCN1） was expressed in the extravillous trophoblasts （EVTs） and decreased in preeclampsia. Its regulatory...

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Bibliographic Details
Published in:Journal of Huazhong University of Science and Technology. Medical sciences 2011-04, Vol.31 (2), p.235-240
Main Author: 陈茜 刘燕燕 徐晓燕 陈汉平
Format: Article
Language:English
Subjects:
Adult
Apoptosis - physiology
Cell Hypoxia
Cell Line
Cell Proliferation
Cobalt - pharmacology
Cysteine-Rich Protein 61 - metabolism
Down-Regulation
Female
Humans
Medicine
Medicine & Public Health
Pre-Eclampsia - physiopathology
Pregnancy
Trophoblasts - pathology
低氧环境
先兆
基因诱导
子痫
滋养层细胞
细胞凋亡
绒毛
缺氧条件
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Summary:During placental development, oxygen environment is not only critical for trophoblasts migration and invasion, but also fundamental for appropriate placental perfusion. Cysteine-rich 61 （Cyr61, CCN1） was expressed in the extravillous trophoblasts （EVTs） and decreased in preeclampsia. Its regulatory properties in human first-trimester extravillous trophoblast cell line （TEV-1 cells） upon a low oxygen tension were investigated. The present study examined functional changes involved in adaptation to hypoxia of the TEV-1 cells, using cobalt chloride （CoCl2） as hypoxic mimic. It was found that hypoxia inhibited growth of TEV-1 cells and induced the increase of cell apoptosis （P0.05）. The Cyr61 expression in human EVTs was transcriptionally induced by CoCl2. Inappropriate EVTs apoptosis has been implicated in the failure of trophoblasts to fully invade and modify the uterine environment and Cyr61 down-regulation, potentially leading to preeclampsia.
ISSN:1672-0733
1993-1352
DOI:10.1007/s11596-011-0259-9