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Analysis of cell-cell junctions in human amnion and chorionic plate affected by chorioamnionitis

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dc.contributor.authorLicini, Caterina
dc.contributor.authorTossetta, Giovanni
dc.contributor.authorAvellini, Chiara
dc.contributor.authorCiarmela, Pasquapina
dc.contributor.authorLorenzi, Teresa
dc.contributor.authorToti, Paolo
dc.contributor.authorGesuita, Rosaria
dc.contributor.authorVoltolini, Chiara
dc.contributor.authorPetraglia, Felice
dc.contributor.authorCastellucci, Mario
dc.contributor.authorMarzioni, Daniela
dc.date.accessioned2021-07-28T10:32:52Z
dc.date.available2021-07-28T10:32:52Z
dc.date.issued2016
dc.description.abstractChorioamnionitis is an acute inflammatory reaction associated with the premature rupture of the fetal membranes. It is caused mainly by invasion of bacteria from the vaginal tract that can penetrate the intact membranes and invade the amnion cavity and the decidua. Tight junctions (TJ) and adherent junctions (AJ) are intercellular junctions crucial for epithelia adhesion and permeability regulation in a wide variety of tissues and organs. Our aim is to investigate if TJ and AJ molecules are involved in human chorioamnionitis. We studied the protein expression (by immunohistochemistry and western blotting) and the mRNA levels (by RT-PCR) of some junction proteins such as Zonula Occludens-1 (ZO-1), occludin, VE-cadherin and βcatenin in fetal membranes from women with chorioamnionitis compared to those membranes derived from idiopathic pregnancies. Western blotting and immunohistochemical data established that occludin expression was decreased in amnion with chorioamnionitis compared to amnion from idiopathic pregnancies. Samples tested for ZO-1, VEcadherin and β-catenin (proteins and mRNAs) showed no differences between idiopathic and pathological membranes. One of the most relevant results is the decrease of occludin in membranes with chorioamnionitis. Since we have previously demonstrated that some cytokines, particularly elevated in the chorioamnionitis, cause the disruption of TJs in placental villi, we suggest that the decrease of occludin in amnion may be the first change that leads to the rupture of the amniotic membrane in this pathology.es
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dc.identifier.citationHistology and histopathology, Vol.31, nº7 (2016)
dc.identifier.doiDOI: 10.14670/HH-11-719
dc.identifier.issn1699-5848
dc.identifier.issn0213-3911
dc.identifier.urihttp://hdl.handle.net/10201/111408
dc.languageenges
dc.relationSin financiación externa a la Universidades
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectTight junctiones
dc.subjectAdherent junctiones
dc.subjectAmniones
dc.subjectChorioamnionitises
dc.subject.otherCDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncologíaes
dc.titleAnalysis of cell-cell junctions in human amnion and chorionic plate affected by chorioamnionitises
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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Histology and histopathology Vol.31, nº7 (2016)