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Loss of GATA4 causes ectopic pancreas in the stomach.

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dc.contributor.authorRodríguez-Seguel, Elisa
dc.contributor.authorVillamayor, Laura
dc.contributor.authorArroyo, Noelia
dc.contributor.authorDe Andrés, Mónica P
dc.contributor.authorReal Arribas, Francisco
dc.contributor.authorMartín, Franz
dc.contributor.authorCano, David A
dc.contributor.authorRojas, Anabel
dc.contributor.funderMinisterio de Ciencia y Universidades (España)es_ES
dc.date.accessioned2024-02-14T10:07:00Z
dc.date.available2024-02-14T10:07:00Z
dc.date.issued2020-04
dc.description.abstractPancreatic heterotopia is defined as pancreatic tissue outside its normal location in the body and anatomically separated from the pancreas. In this work we have analyzed the stomach glandular epithelium of Gata4 flox/flox ; Pdx1-Cre mice (Gata4KO mice). We found that Gata4KO glandular epithelium displays an atypical morphology similar to the cornified squamous epithelium and exhibits upregulation of forestomach markers. The developing gastric units fail to form properly, and the glandular epithelial cells do not express markers of gastric gland in the absence of GATA4. Of interest, the developing glands of the Gata4KO stomach express pancreatic cell markers. Furthermore, a mass of pancreatic tissue located in the subserosa of the Gata4KO stomach is observed at adult stages. Heterotopic pancreas found in Gata4-deficient mice contains all three pancreatic cell lineages: ductal, acinar, and endocrine. Moreover, Gata4 expression is downregulated in ectopic pancreatic tissue of some human biopsy samples. © 2019 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.es_ES
dc.description.peerreviewedSíes_ES
dc.description.sponsorshipWe thank Antonio Cardenas and Ana Belen Hitos for their technical assistance. ER-S. was supported by a 'Juan de la Cierva' postdoctoral fellowship from the Spanish Ministry of Economy and Competitiveness (IJCI-2014-19251). LV was supported by a contract from Spanish Ministry of Economy and Competitiveness (RYC-2013-14533). This work was supported by grants from the Spanish Ministry of Economy and Competitiveness BFU2017-82497-P to AR, ISCIII-Subdireccion General de Evaluacion y Fomento de la Investigacion co-funded with Fondos FEDER, PI16/00175 to DAC, the Andalusian Ministry of Science and Innovation CTS-7478 to DAC, and grant SAF2015-70553-R to FXR. CNIO is supported by the "Ministerio de Ciencia, Innovacion y Universidades" as a Centro de Excelencia Severo Ochoa (SEV-2015-0510). This research has been conducted using samples from the HUVR-IBiS Biobank (Andalusian Public Health System Biobank and ISCIII-Red de Biobancos PT17/0015/0041). The authors would like to thank Carolina Castilla and Fernando Carmona (HUVR-IBiS Biobank) for their outstanding technical help.es_ES
dc.format.number4es_ES
dc.format.page362es_ES
dc.format.volume250es_ES
dc.identifier.citationJ Pathol . 2020 ;250(4):362-373es_ES
dc.identifier.doi10.1002/path.5378es_ES
dc.identifier.e-issn1096-9896es_ES
dc.identifier.journalThe Journal of pathologyes_ES
dc.identifier.pubmedID31875961es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/18195
dc.language.isoenges_ES
dc.publisherWileyes_ES
dc.relation.projectFISinfo:eu-repo/grantAgreement/ES/PI16/00175es_ES
dc.relation.publisherversionhttps://doi.org/10.1002/path.5378es_ES
dc.repisalud.institucionCNIOes_ES
dc.repisalud.orgCNIOCNIO::Grupos de investigación::Grupo de Carcinogénesis Epiteliales_ES
dc.rights.accessRightsopen accesses_ES
dc.rights.licenseAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subject.meshAnimalses_ES
dc.subject.meshCell Differentiationes_ES
dc.subject.meshEpithelial Cellses_ES
dc.subject.meshGATA4 Transcription Factores_ES
dc.subject.meshGastric Mucosaes_ES
dc.subject.meshGene Expression Regulation, Developmentales_ES
dc.subject.meshHumanses_ES
dc.subject.meshMice, Transgenices_ES
dc.subject.meshOrganogenesises_ES
dc.subject.meshPancreases_ES
dc.titleLoss of GATA4 causes ectopic pancreas in the stomach.es_ES
dc.typejournal articlees_ES
dc.type.hasVersionAOes_ES
dspace.entity.typePublication
relation.isAuthorOfPublication62d13a40-e75d-49b1-bb0a-f54a4146ad3e
relation.isAuthorOfPublication.latestForDiscovery62d13a40-e75d-49b1-bb0a-f54a4146ad3e
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