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Article: Wnt activation downregulates olfactomedin-1 in Fallopian tubal epithelial cells: A microenvironment predisposed to tubal ectopic pregnancy

TitleWnt activation downregulates olfactomedin-1 in Fallopian tubal epithelial cells: A microenvironment predisposed to tubal ectopic pregnancy
Authors
KeywordsFallopian tube
olfactomedin-1
tubal ectopic pregnancy
Wnt signaling
Issue Date2012
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/labinvest/
Citation
Laboratory Investigation, 2012, v. 92 n. 2, p. 256-264 How to Cite?
Abstract
Ectopic pregnancy (EP) occurs when the embryo fails to transit to the uterus and attach to the luminal epithelium of the Fallopian tube (FT). Tubal EP is a common gynecological emergency and more than 95% of EP occurs in the ampullary region of the FT. In humans, Wnt activation and downregulation of olfactomedin-1 (Olfm-1) occur in the receptive endometrium and coincided with embryo implantation in vivo. Whether similar molecular changes happen in the FT leading to EP remains unclear. We hypothesized that activation of Wnt signaling downregulates Olfm-1 expression predisposes to EP. We investigated the spatiotemporal expression of Olfm-1 in FT from non-pregnant women and women with EP, and used a novel trophoblastic spheroid (embryo surrogate)-FT epithelial cell co-culture model (JAr and OE-E6/E7 cells) to study the role of Olfm-1 on spheroid attachment. Olfm-1 mRNA expression in the ampullary region of non-pregnant FT was higher (P0.05) in the follicular phase than in the luteal phase. Ampullary tubal Olfm-1 expression was lower in FT from women with EP compared to normal controls at the luteal phase (histological scoring (H-SCORE)1.30.2 vs 2.40.5; P0.05). Treatment of OE-E6/E7 with recombinant Olfm-1 (0.2-5 g/ml) suppressed spheroid attachment to OE-E6/E7 cells, while activation of Wnt-signaling pathway by Wnt3a or LiCl reduced endogenous Olfm-1 expression and increased spheroid attachment. Conversely, suppression of Olfm-1 expression by RNAi increased spheroid attachment to OE-E6/E7 cells. Taken together, Wnt activation suppresses Olfm-1 expression, and this may predispose a favorable microenvironment of the retained embryo in the FT, leading to EP in humans. © 2012 USCAP, Inc All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/152950
ISSN
2013 Impact Factor: 3.828
PubMed Central ID
ISI Accession Number ID
References

 

Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine
  2. University of Peradeniya
  3. University of Edinburgh
DC FieldValueLanguage
dc.contributor.authorKodithuwakku, SPen_HK
dc.contributor.authorPang, RTKen_HK
dc.contributor.authorNg, EHYen_HK
dc.contributor.authorCheung, ANYen_HK
dc.contributor.authorHorne, AWen_HK
dc.contributor.authorHo, PCen_HK
dc.contributor.authorYeung, WSBen_HK
dc.contributor.authorLee, KFen_HK
dc.date.accessioned2012-07-16T09:52:57Z-
dc.date.available2012-07-16T09:52:57Z-
dc.date.issued2012en_HK
dc.identifier.citationLaboratory Investigation, 2012, v. 92 n. 2, p. 256-264en_HK
dc.identifier.issn0023-6837en_HK
dc.identifier.urihttp://hdl.handle.net/10722/152950-
dc.description.abstractEctopic pregnancy (EP) occurs when the embryo fails to transit to the uterus and attach to the luminal epithelium of the Fallopian tube (FT). Tubal EP is a common gynecological emergency and more than 95% of EP occurs in the ampullary region of the FT. In humans, Wnt activation and downregulation of olfactomedin-1 (Olfm-1) occur in the receptive endometrium and coincided with embryo implantation in vivo. Whether similar molecular changes happen in the FT leading to EP remains unclear. We hypothesized that activation of Wnt signaling downregulates Olfm-1 expression predisposes to EP. We investigated the spatiotemporal expression of Olfm-1 in FT from non-pregnant women and women with EP, and used a novel trophoblastic spheroid (embryo surrogate)-FT epithelial cell co-culture model (JAr and OE-E6/E7 cells) to study the role of Olfm-1 on spheroid attachment. Olfm-1 mRNA expression in the ampullary region of non-pregnant FT was higher (P0.05) in the follicular phase than in the luteal phase. Ampullary tubal Olfm-1 expression was lower in FT from women with EP compared to normal controls at the luteal phase (histological scoring (H-SCORE)1.30.2 vs 2.40.5; P0.05). Treatment of OE-E6/E7 with recombinant Olfm-1 (0.2-5 g/ml) suppressed spheroid attachment to OE-E6/E7 cells, while activation of Wnt-signaling pathway by Wnt3a or LiCl reduced endogenous Olfm-1 expression and increased spheroid attachment. Conversely, suppression of Olfm-1 expression by RNAi increased spheroid attachment to OE-E6/E7 cells. Taken together, Wnt activation suppresses Olfm-1 expression, and this may predispose a favorable microenvironment of the retained embryo in the FT, leading to EP in humans. © 2012 USCAP, Inc All rights reserved.en_HK
dc.languageengen_US
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/labinvest/en_HK
dc.relation.ispartofLaboratory Investigationen_HK
dc.subjectFallopian tubeen_HK
dc.subjectolfactomedin-1en_HK
dc.subjecttubal ectopic pregnancyen_HK
dc.subjectWnt signalingen_HK
dc.subject.meshExtracellular Matrix Proteins - physiology-
dc.subject.meshFallopian Tubes - cytology - metabolism-
dc.subject.meshGlycoproteins - physiology-
dc.subject.meshPregnancy, Tubal - physiopathology-
dc.subject.meshWnt Proteins - physiology-
dc.titleWnt activation downregulates olfactomedin-1 in Fallopian tubal epithelial cells: A microenvironment predisposed to tubal ectopic pregnancyen_HK
dc.typeArticleen_HK
dc.identifier.emailPang, RTK: rtkpang@hku.hken_HK
dc.identifier.emailNg, EHY: nghye@hku.hken_HK
dc.identifier.emailCheung, ANY: anycheun@hkucc.hku.hken_HK
dc.identifier.emailHo, PC: pcho@hku.hken_HK
dc.identifier.emailLee, KF: ckflee@hku.hken_HK
dc.identifier.authorityPang, RTK=rp01761en_HK
dc.identifier.authorityNg, EHY=rp00426en_HK
dc.identifier.authorityCheung, ANY=rp00542en_HK
dc.identifier.authorityHo, PC=rp00325en_HK
dc.identifier.authorityLee, KF=rp00458en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1038/labinvest.2011.148en_HK
dc.identifier.pmid21968811en_HK
dc.identifier.pmcidPMC3272473-
dc.identifier.scopuseid_2-s2.0-84863063431en_HK
dc.identifier.hkuros201421en_US
dc.identifier.hkuros211344-
dc.identifier.hkuros227376-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84863063431&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume92en_HK
dc.identifier.issue2en_HK
dc.identifier.spage256en_HK
dc.identifier.epage264en_HK
dc.identifier.isiWOS:000299799700009-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridKodithuwakku, SP=8939085200en_HK
dc.identifier.scopusauthoridPang, RTK=7004376636en_HK
dc.identifier.scopusauthoridNg, EHY=35238184300en_HK
dc.identifier.scopusauthoridCheung, ANY=54927484100en_HK
dc.identifier.scopusauthoridHorne, AW=55148033300en_HK
dc.identifier.scopusauthoridHo, PC=7402211440en_HK
dc.identifier.scopusauthoridYeung, WSB=55763794908en_HK
dc.identifier.scopusauthoridLee, KF=26643097500en_HK
dc.identifier.citeulike9866230-
dc.customcontrol.immutablesml 130626-

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