Effect of RU486 on apoptosis and p53 expression at the boundary of fetal-maternal interface of rhesus monkey (Macaca mulatta).
- Author:
Peng WEI
1
,
2
;
E-mail: LIUYX@PANDA.IOZ.AC.CN
;
Shi-Xin TAO
;
Xue-Sen ZHANG
;
Zhao-Yuan HU
;
Liu YI-XUN
Author Information
1. State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100080 China
2. E-mail: liuyx@panda.ioz.ac.cn
- Publication Type:Journal Article
- MeSH:
Abortifacient Agents, Steroidal;
pharmacology;
Animals;
Apoptosis;
drug effects;
Chorionic Villi;
pathology;
Female;
Macaca mulatta;
Mifepristone;
pharmacology;
Placentation;
drug effects;
physiology;
Pregnancy;
Tumor Suppressor Protein p53;
biosynthesis;
genetics
- From:
Acta Physiologica Sinica
2004;56(1):60-65
- CountryChina
- Language:Chinese
-
Abstract:
Primate placentation involves a series of cell proliferation, immigration and apoptosis which account for the progressive tissue remodelling at the implantation site. p53 is an important proto-oncogene involved in the regulation of cell-cycle and apoptosis. To study the effect of RU486 on apoptosis and expression of p53 at the fetal-maternal interface, the location of apoptotic cells and expression of p53 were examined using in situ 3'-end labeling method, immunohistochemistry and Western blot assay at the fetal-maternal interface of normal and RU486 treated rhesus monkey. Western blot analysis showed the specificity of the anti-human antibody used with the monkey tissue. In the placental villi, the apoptotic nuclei were observed mainly in the syncytiotrophoblast and part of the cytotrophoblast within the cell column; p53 protein was detected mainly in the cytotrophoblast. In the endometrium, positive signals for apoptosis and p53 were detected in some stromal cells. After two days of mifepristone treatment, the apoptotic cells increased significantly in both placental villi and endometrium. In the villi, the increased apoptotic nuclei were mainly localized to the cytotrophoblast. At the same time, p53-positive nuclei also increased in both villous cytotrophoblast cells and endometrial stromal cells, after the treatment of RU486. These results suggest that apoptosis and expression of p53 are essential in regulating trophoblastic homeostasis by controlling its proliferation in normal placenta, whereas the up-regulation of p53 protein may play an important role in apoptosis that happens at the fetal-maternal interface induced by RU486.
