Please use this identifier to cite or link to this item: https://repositorio.uca.edu.ar/handle/123456789/8915
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dc.contributor.authorMassip Copiz, María Macarenaes
dc.contributor.authorClauzure, Mariángeleses
dc.contributor.authorValdivieso, Ángel Gabrieles
dc.contributor.authorSanta Coloma, Tomás Antonioes
dc.date.accessioned2019-10-28T18:38:45Z-
dc.date.available2019-10-28T18:38:45Z-
dc.date.issued2018-
dc.identifier.citationMassip‐Copiz M, Clauzure M, Valdivieso ÁG, Santa‐Coloma TA. Epiregulin (EREG) is upregulated through an IL-1β autocrine loop in Caco-2 epithelial cells with reduced CFTR function [en línea]. Journal of Cellular Biochemistry. 2018;119(3):2911-2922. doi:10.1002/jcb.26483 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/8915es
dc.identifier.issn0730-2312 (impreso)-
dc.identifier.issn1097-4644 (online)-
dc.identifier.urihttps://repositorio.uca.edu.ar/handle/123456789/8915-
dc.description.abstractAbstract: CFTR is a cAMP-regulated chloride channel, whose mutations produce cystic fibrosis. The impairment of CFTR activity increases the intracellular Cl- concentration, which in turn produces an increased interleukin-1β (IL-1β) secretion. The secreted IL-1β then induces an autocrine positive feedback loop, further stimulating IL-1β priming and secretion. Since IL-1β can transactivate the epidermal growth factor receptor (EGFR), we study here the levels of expression for different EGFR ligands in Caco-2/pRS26 cells (expressing shRNA against CFTR resulting in a reduced CFTR expression and activity). The epiregulin (EREG), amphiregulin (AREG), and heparin binding EGF like growth factor (HBEGF) mRNAs, were found overexpressed in Caco-2/pRS26 cells. The EREG mRNA had the highest differential expression and was further characterized. In agreement with its mRNA levels, Western blots (WB) showed increased EREG levels in CFTR-impaired cells. In addition, EREG mRNA and protein levels were stimulated by incubation with exogenous IL-1β and inhibited by the Interleukin 1 receptor type I (IL1R1) antagonist IL1RN, suggesting that the overexpression of EREG is a consequence of the autocrine IL-1β loop previously described for these cells. In addition, the JNK inhibitor SP600125, and the EGFR inhibitors AG1478 and PD168393, also had an inhibitory effect on EREG expression, suggesting that EGFR, activated in Caco-2/pRS26 cells, is involved in the observed EREG upregulation. In conclusion, in Caco-2 CFTR-shRNA cells, the EGFR ligand EREG is overexpressed due to an active IL-1β autocrine loop that indirectly activates EGFR, constituting new signaling effectors for the CFTR signaling pathway, downstream of CFTR, Cl- , and IL-1β.es
dc.description.sponsorshipAgencia Nacional de Promoción Científica y Tecnológicaes
dc.description.sponsorshipConsejo Nacional de Investigaciones Científicas y Técnicases
dc.description.sponsorshipPontificia Universidad Católica Argentinaes
dc.formatapplication/pdfes
dc.language.isoenges
dc.publisherWileyes
dc.rightsAcceso abierto*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.sourceJournal of Cellular Biochemistry. 2018;119(3):2911-2922es
dc.subjectPROTEINASes
dc.subjectFIBROSIS QUISTICAes
dc.subjectGENES CFTR DEPENDIENTESes
dc.subjectCELULAS EPITELIALESes
dc.subjectFISIOLOGIAes
dc.titleEpiregulin (EREG) is upregulated through an IL-1β autocrine loop in Caco-2 epithelial cells with reduced CFTR functiones
dc.typeArtículoes
dc.identifier.doi10.1002/jcb.26483-
dc.identifier.pmid29091309-
uca.disciplinaMEDICINAes
uca.issnrd1es
uca.affiliationFil: Massip Copiz, María Macarena. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentinaes
uca.affiliationFil: Massip Copiz, María Macarena. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentinaes
uca.affiliationFil: Clauzure, Mariángeles. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentinaes
uca.affiliationFil: Clauzure, Mariángeles. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentinaes
uca.affiliationFil: Valdivieso, Ángel Gabriel. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentinaes
uca.affiliationFil: Valdivieso, Ángel Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentinaes
uca.affiliationFil: Santa Coloma, Tomás Antonio. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentinaes
uca.affiliationFil: Santa Coloma, Tomás Antonio. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentinaes
uca.versionacceptedVersiones
item.fulltextWith Fulltext-
item.grantfulltextopen-
item.languageiso639-1en-
crisitem.author.deptInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.deptLaboratorio de Biología Celular y Molecular-
crisitem.author.deptLaboratorio de Biología Celular y Molecular-
crisitem.author.deptInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.deptLaboratorio de Biología Celular y Molecular-
crisitem.author.deptConsejo Nacional de Investigaciones Científicas y Técnicas-
crisitem.author.deptInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.deptLaboratorio de Biología Celular y Molecular-
crisitem.author.deptLaboratorio de Nanotecnología-
crisitem.author.deptConsejo Nacional de Investigaciones Científicas y Técnicas-
crisitem.author.orcid0000-0002-3266-1095-
crisitem.author.parentorgFacultad de Ciencias Médicas-
crisitem.author.parentorgInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.parentorgInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.parentorgFacultad de Ciencias Médicas-
crisitem.author.parentorgInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.parentorgFacultad de Ciencias Médicas-
crisitem.author.parentorgInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.parentorgInstituto de Investigaciones Biomédicas - BIOMED-
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