Human endometrial CD98 is essential for blastocyst adhesion.

<h4>Background</h4>Understanding the molecular basis of embryonic implantation is of great clinical and biological relevance. Little is currently known about the adhesion receptors that determine endometrial receptivity for embryonic implantation in humans.<h4>Methods and principal...

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Autores principales: Francisco Domínguez, Carlos Simón, Alicia Quiñonero, Miguel Ángel Ramírez, Elena González-Muñoz, Hans Burghardt, Ana Cervero, Sebastián Martínez, Antonio Pellicer, Manuel Palacín, Francisco Sánchez-Madrid, María Yáñez-Mó
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Publicado: Public Library of Science (PLoS) 2010
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Acceso en línea:https://doaj.org/article/b473190798e84c9183c6ecbb1fd4ee27
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spelling oai:doaj.org-article:b473190798e84c9183c6ecbb1fd4ee272021-11-18T07:03:16ZHuman endometrial CD98 is essential for blastocyst adhesion.1932-620310.1371/journal.pone.0013380https://doaj.org/article/b473190798e84c9183c6ecbb1fd4ee272010-10-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20976164/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Understanding the molecular basis of embryonic implantation is of great clinical and biological relevance. Little is currently known about the adhesion receptors that determine endometrial receptivity for embryonic implantation in humans.<h4>Methods and principal findings</h4>Using two human endometrial cell lines characterized by low and high receptivity, we identified the membrane receptor CD98 as a novel molecule selectively and significantly associated with the receptive phenotype. In human endometrial samples, CD98 was the only molecule studied whose expression was restricted to the implantation window in human endometrial tissue. CD98 expression was restricted to the apical surface and included in tetraspanin-enriched microdomains of primary endometrial epithelial cells, as demonstrated by the biochemical association between CD98 and tetraspanin CD9. CD98 expression was induced in vitro by treatment of primary endometrial epithelial cells with human chorionic gonadotropin, 17-β-estradiol, LIF or EGF. Endometrial overexpression of CD98 or tetraspanin CD9 greatly enhanced mouse blastocyst adhesion, while their siRNA-mediated depletion reduced the blastocyst adhesion rate.<h4>Conclusions</h4>These results indicate that CD98, a component of tetraspanin-enriched microdomains, appears to be an important determinant of human endometrial receptivity during the implantation window.Francisco DomínguezCarlos SimónAlicia QuiñoneroMiguel Ángel RamírezElena González-MuñozHans BurghardtAna CerveroSebastián MartínezAntonio PellicerManuel PalacínFrancisco Sánchez-MadridMaría Yáñez-MóPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 5, Iss 10, p e13380 (2010)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Francisco Domínguez
Carlos Simón
Alicia Quiñonero
Miguel Ángel Ramírez
Elena González-Muñoz
Hans Burghardt
Ana Cervero
Sebastián Martínez
Antonio Pellicer
Manuel Palacín
Francisco Sánchez-Madrid
María Yáñez-Mó
Human endometrial CD98 is essential for blastocyst adhesion.
description <h4>Background</h4>Understanding the molecular basis of embryonic implantation is of great clinical and biological relevance. Little is currently known about the adhesion receptors that determine endometrial receptivity for embryonic implantation in humans.<h4>Methods and principal findings</h4>Using two human endometrial cell lines characterized by low and high receptivity, we identified the membrane receptor CD98 as a novel molecule selectively and significantly associated with the receptive phenotype. In human endometrial samples, CD98 was the only molecule studied whose expression was restricted to the implantation window in human endometrial tissue. CD98 expression was restricted to the apical surface and included in tetraspanin-enriched microdomains of primary endometrial epithelial cells, as demonstrated by the biochemical association between CD98 and tetraspanin CD9. CD98 expression was induced in vitro by treatment of primary endometrial epithelial cells with human chorionic gonadotropin, 17-β-estradiol, LIF or EGF. Endometrial overexpression of CD98 or tetraspanin CD9 greatly enhanced mouse blastocyst adhesion, while their siRNA-mediated depletion reduced the blastocyst adhesion rate.<h4>Conclusions</h4>These results indicate that CD98, a component of tetraspanin-enriched microdomains, appears to be an important determinant of human endometrial receptivity during the implantation window.
format article
author Francisco Domínguez
Carlos Simón
Alicia Quiñonero
Miguel Ángel Ramírez
Elena González-Muñoz
Hans Burghardt
Ana Cervero
Sebastián Martínez
Antonio Pellicer
Manuel Palacín
Francisco Sánchez-Madrid
María Yáñez-Mó
author_facet Francisco Domínguez
Carlos Simón
Alicia Quiñonero
Miguel Ángel Ramírez
Elena González-Muñoz
Hans Burghardt
Ana Cervero
Sebastián Martínez
Antonio Pellicer
Manuel Palacín
Francisco Sánchez-Madrid
María Yáñez-Mó
author_sort Francisco Domínguez
title Human endometrial CD98 is essential for blastocyst adhesion.
title_short Human endometrial CD98 is essential for blastocyst adhesion.
title_full Human endometrial CD98 is essential for blastocyst adhesion.
title_fullStr Human endometrial CD98 is essential for blastocyst adhesion.
title_full_unstemmed Human endometrial CD98 is essential for blastocyst adhesion.
title_sort human endometrial cd98 is essential for blastocyst adhesion.
publisher Public Library of Science (PLoS)
publishDate 2010
url https://doaj.org/article/b473190798e84c9183c6ecbb1fd4ee27
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