Chen Xi, Liu Yanyan, Xu Xiaoyan, Chen Hanping
Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
J Huazhong Univ Sci Technolog Med Sci. 2011 Apr;31(2):235-240. doi: 10.1007/s11596-011-0259-9. Epub 2011 Apr 20.
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 (CoCl(2)) as hypoxic mimic. It was found that hypoxia inhibited growth of TEV-1 cells and induced the increase of cell apoptosis (P<0.05). The Cyr61 expression in human EVTs was transcriptionally induced by CoCl(2). 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.
在胎盘发育过程中，氧环境不仅对滋养层细胞的迁移和侵袭至关重要，而且对胎盘的适当灌注也至关重要。富含半胱氨酸的61（Cyr61，CCN1）在绒毛外滋养层细胞（EVT）中表达，在子痫前期中表达降低。研究了其在低氧张力下人早孕绒毛外滋养层细胞系（TEV-1细胞）中的调节特性。本研究使用氯化钴（CoCl₂）作为缺氧模拟物，检测了TEV-1细胞适应缺氧所涉及的功能变化。结果发现，缺氧抑制了TEV-1细胞的生长并诱导细胞凋亡增加（P<0.05）。CoCl₂可转录诱导人EVT中Cyr61的表达。不适当的EVT凋亡与滋养层细胞未能完全侵入和改变子宫环境以及Cyr61下调有关，这可能导致子痫前期。
