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Regular article |
a Instituto Valenciano de Infertilidad, 46020 Valencia, Spain
b Department of Pediatrics, Obstetrics, and Gynecology and
c Department of Biochemistry and Molecular Biology, University of Valencia, 46010 Valencia, Spain
d OBST 5330 Research Unit, Université de Louvain Medical School, Brussels, Belgium
ABSTRACT
The implanting blastocyst must appose and adhere to the endometrial epithelium and, subsequently, invade it. Locally regulated uterine epithelial apoptosis induced by the embryo is a crucial step of the epithelial invasion in rodents. To address the physiological relevance of this process in humans, we investigated the effect of single human blastocysts on the regulation of apoptosis in cultured human endometrial epithelial cells (hEEC) in both apposition and adhesion phases of implantation. Here, we report a co-ordinated embryonic regulation of hEEC apoptosis. In the apposition phase, the presence of a blastocyst rescues hEEC from the apoptotic pathway. However, when the human blastocyst adheres to the hEEC monolayer, it induces a paracrine apoptotic reaction. Fas ligand (Fas-L) was present at the embryonic trophoectoderm. Fas was localized at the apical cell surface of hEEC, and flow cytometry revealed that 60% of hEEC express Fas. Neutralizing adhesion assays revealed that the Fas/Fas-L death system may be an important mechanism to cross the epithelial barrier, which is crucial for embryonic adhesion, and the manipulation of this system could have potential clinical implications as an interceptive mechanism.
First decision: 16 December 1999.
1 Supported by IVI Foundation and FISss 00/0643 grant from the Spanish Government, Ministerio de Sanidad y Consumo, Madrid.
2 Correspondence: Carlos Simón, Instituto Valenciano de Infertilidad. Guardia Civil 23, 46020 Valencia, Spain. FAX: 34 963694735; csimon{at}interbook.net
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