Mol. Hum. Reprod. Advance Access originally published online on March 4, 2005
Molecular Human Reproduction 2005 11(4):245-251; doi:10.1093/molehr/gah147
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Differentiation of endometrial stromal cells in vitro: down-regulation of suppression of the cell cycle inhibitor p57 by HOXA10?
1Reproductive Medicine Center and 2Neuorologic Department, Tongji Hospital, Tongji Medicine College, Huazhong University of Science and Technology, Wuhan, 430030, People's Republic of China
3 To whom correspondence should be addressed. E-mail: zhu_guijin{at}sina.com
Decidualization is a critical step during embryo implantation that is characterized by the differentiation of endometrial stromal cells (ESC) into decidua cells. However, the mechanism of differentiation remains largely unknown. Previously, it has been shown that the null function of homeo box A10 (HOXA10) causes defects in both implantation and decidualization, suggesting that the HOXA10 signalling pathway is likely to be involved in uterine decidualization. In the present study, we determined the expression and subcellular distribution of HOXA10 and its downstream molecule, p57, in ESC during in vitro decidualization induced by a combination of 8-bromo-cAMP and medroxyprogesterone acetate. We demonstrated that the HOXA10 was down-regulated while in contrast, p57 was up-regulated in the process of decidualization. Immunocytochemistry and transient expression of the HOXA10 tagged with green fluorescence protein revealed that there were no differences in the HOXA10 subcellular localization between the induced and non-induced ESC. Our results suggest that the down-regulation of HOXA10 may contribute to increased p57 and that up-regulation of p57 likely plays an important role in ESC differentiation in the process of decidualization. The progesterone receptor pathway may participate in promoting ESC to exit the cell cycle and enter differentiation.
Key words: embryonic implantation/decidua/homeo box A10 protein/human/p57KIP2
* These authors made an equal contribution to the paper.
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