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Article: 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) suppresses spheroids attachment on endometrial epithelial cells through the down-regulation of the Wnt-signaling pathway

Title2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) suppresses spheroids attachment on endometrial epithelial cells through the down-regulation of the Wnt-signaling pathway
Authors
KeywordsAttachment
Canonical Wnt-signaling
Endometrium
Implantation
Spheroids
TCDD
Issue Date2012
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/reprotox
Citation
Reproductive Toxicology, 2012, v. 33 n. 1, p. 60-66 How to Cite?
AbstractThe environmental toxicant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) affects embryo development, implantation and fertility in humans. The underlying molecular mechanism by which TCDD suppresses implantation remains largely unknown. We used the trophoblastic spheroids (embryo surrogate)-endometrial cells co-culture assay to study the attachment of trophoblastic spheroids (BeWo and Jeg-3) onto the endometrial epithelial (RL95-2 and Ishikawa) cells. TCDD dose-dependently induced cytochrome P450 1A1 (Cyp1A1) expression in trophoblastic and endometrial epithelial cells. Moreover, TCDD at 1 and 10. nM suppressed β-catenin (a Wnt-signaling molecule) and E-cadherin expression, as well as spheroids attachment onto endometrial cells. Interestingly, activation of the canonical Wnt-signaling pathway via Wnt3a or lithium chloride reverted the suppressive effect of TCDD on β-catenin and E-cadherin expressions in the BeWo and RL95-2 cells, and restored the spheroids attachment rate to be comparable to the untreated controls. Taken together, TCDD induces Cyp1A1 expression, modulates the Wnt-signaling pathway and suppresses spheroids attachment onto endometrial cells. © 2011 Elsevier Inc.
Persistent Identifierhttp://hdl.handle.net/10722/173372
ISSN
2021 Impact Factor: 3.421
2020 SCImago Journal Rankings: 0.845
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTsang, Hen_US
dc.contributor.authorCheung, TYen_US
dc.contributor.authorKodithuwakku, SPen_US
dc.contributor.authorChai, Jen_US
dc.contributor.authorYeung, WSBen_US
dc.contributor.authorWong, CKCen_US
dc.contributor.authorLee, KFen_US
dc.date.accessioned2012-10-30T06:29:42Z-
dc.date.available2012-10-30T06:29:42Z-
dc.date.issued2012en_US
dc.identifier.citationReproductive Toxicology, 2012, v. 33 n. 1, p. 60-66en_US
dc.identifier.issn0890-6238en_US
dc.identifier.urihttp://hdl.handle.net/10722/173372-
dc.description.abstractThe environmental toxicant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) affects embryo development, implantation and fertility in humans. The underlying molecular mechanism by which TCDD suppresses implantation remains largely unknown. We used the trophoblastic spheroids (embryo surrogate)-endometrial cells co-culture assay to study the attachment of trophoblastic spheroids (BeWo and Jeg-3) onto the endometrial epithelial (RL95-2 and Ishikawa) cells. TCDD dose-dependently induced cytochrome P450 1A1 (Cyp1A1) expression in trophoblastic and endometrial epithelial cells. Moreover, TCDD at 1 and 10. nM suppressed β-catenin (a Wnt-signaling molecule) and E-cadherin expression, as well as spheroids attachment onto endometrial cells. Interestingly, activation of the canonical Wnt-signaling pathway via Wnt3a or lithium chloride reverted the suppressive effect of TCDD on β-catenin and E-cadherin expressions in the BeWo and RL95-2 cells, and restored the spheroids attachment rate to be comparable to the untreated controls. Taken together, TCDD induces Cyp1A1 expression, modulates the Wnt-signaling pathway and suppresses spheroids attachment onto endometrial cells. © 2011 Elsevier Inc.en_US
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/reprotoxen_US
dc.relation.ispartofReproductive Toxicologyen_US
dc.rightsNOTICE: this is the author’s version of a work that was accepted for publication in Reproductive Toxicology. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Reproductive Toxicology, 2012, v. 33 n. 1, p. 60-66. DOI: 10.1016/j.reprotox.2011.11.002-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectAttachment-
dc.subjectCanonical Wnt-signaling-
dc.subjectEndometrium-
dc.subjectImplantation-
dc.subjectSpheroids-
dc.subjectTCDD-
dc.subject.meshBasic Helix-Loop-Helix Transcription Factors - Drug Effects - Metabolismen_US
dc.subject.meshCadherins - Metabolismen_US
dc.subject.meshCell Adhesion - Drug Effectsen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshCoculture Techniquesen_US
dc.subject.meshCytochrome P-450 Cyp1a1 - Biosynthesisen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshEmbryo Implantation - Drug Effectsen_US
dc.subject.meshEndometrium - Drug Effects - Metabolism - Pathologyen_US
dc.subject.meshEnvironmental Pollutants - Toxicityen_US
dc.subject.meshEnzyme Inductionen_US
dc.subject.meshEpithelial Cells - Drug Effects - Metabolism - Pathologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshHumansen_US
dc.subject.meshReceptors, Aryl Hydrocarbon - Drug Effects - Metabolismen_US
dc.subject.meshSpheroids, Cellularen_US
dc.subject.meshTetrachlorodibenzodioxin - Toxicityen_US
dc.subject.meshTrophoblasts - Drug Effects - Metabolism - Pathologyen_US
dc.subject.meshWnt Signaling Pathway - Drug Effectsen_US
dc.subject.meshBeta Catenin - Metabolismen_US
dc.title2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) suppresses spheroids attachment on endometrial epithelial cells through the down-regulation of the Wnt-signaling pathwayen_US
dc.typeArticleen_US
dc.identifier.emailChai, J:jchai@hkucc.hku.hken_US
dc.identifier.emailYeung, WSB:wsbyeung@hkucc.hku.hken_US
dc.identifier.emailLee, KF:ckflee@hku.hken_US
dc.identifier.authorityChai, J=rp00241en_US
dc.identifier.authorityYeung, WSB=rp00331en_US
dc.identifier.authorityLee, KF=rp00458en_US
dc.description.naturepostprinten_US
dc.identifier.doi10.1016/j.reprotox.2011.11.002en_US
dc.identifier.pmid22134133-
dc.identifier.scopuseid_2-s2.0-84856704954en_US
dc.identifier.hkuros205913-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84856704954&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume33en_US
dc.identifier.issue1en_US
dc.identifier.spage60en_US
dc.identifier.epage66en_US
dc.identifier.eissn1873-1708-
dc.identifier.isiWOS:000300762700008-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridTsang, H=54418099800en_US
dc.identifier.scopusauthoridCheung, TY=54417042300en_US
dc.identifier.scopusauthoridKodithuwakku, SP=8939085200en_US
dc.identifier.scopusauthoridChai, J=35200414100en_US
dc.identifier.scopusauthoridYeung, WSB=7102370745en_US
dc.identifier.scopusauthoridWong, CKC=35276549400en_US
dc.identifier.scopusauthoridLee, KF=26643097500en_US
dc.identifier.citeulike10086741-
dc.identifier.issnl0890-6238-

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