Stage-specific integration of maternal and embryonic peroxisome proliferator-activated receptor delta signaling is critical to pregnancy success.

Détails

ID Serval
serval:BIB_EAEE8C8BE8B8
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Stage-specific integration of maternal and embryonic peroxisome proliferator-activated receptor delta signaling is critical to pregnancy success.
Périodique
Journal of Biological Chemistry
Auteur⸱e⸱s
Wang H., Xie H., Sun X., Tranguch S., Zhang H., Jia X., Wang D., Das S.K., Desvergne B., Wahli W., DuBois R.N., Dey S.K.
ISSN
0021-9258[print], 0021-9258[linking]
Statut éditorial
Publié
Date de publication
2007
Peer-reviewed
Oui
Volume
282
Numéro
52
Pages
37770-37782
Langue
anglais
Résumé
Successful pregnancy depends on well coordinated developmental events involving both maternal and embryonic components. Although a host of signaling pathways participate in implantation, decidualization, and placentation, whether there is a common molecular link that coordinates these processes remains unknown. By exploiting genetic, molecular, pharmacological, and physiological approaches, we show here that the nuclear transcription factor peroxisome proliferator-activated receptor (PPAR) delta plays a central role at various stages of pregnancy, whereas maternal PPARdelta is critical to implantation and decidualization, and embryonic PPARdelta is vital for placentation. Using trophoblast stem cells, we further elucidate that a reciprocal relationship between PPARdelta-AKT and leukemia inhibitory factor-STAT3 signaling pathways serves as a cell lineage sensor to direct trophoblast cell fates during placentation. This novel finding of stage-specific integration of maternal and embryonic PPARdelta signaling provides evidence that PPARdelta is a molecular link that coordinates implantation, decidualization, and placentation crucial to pregnancy success. This study is clinically relevant because deferral of on time implantation leads to spontaneous pregnancy loss, and defective trophoblast invasion is one cause of preeclampsia in humans.
Mots-clé
Animals, Decidua/metabolism, Embryo Implantation, Female, Fertilization, Gene Expression Regulation, Developmental, Mice, Mice, Inbred C57BL, Mice, Transgenic, Ovulation, PPAR delta/metabolism, Placenta/metabolism, Pregnancy, Pregnancy, Animal/physiology, STAT3 Transcription Factor/physiology, Signal Transduction, Stem Cells/cytology, Time Factors, Trophoblasts/metabolism
Pubmed
Web of science
Open Access
Oui
Création de la notice
24/01/2008 16:26
Dernière modification de la notice
20/08/2019 17:13
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