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dc.contributor.authorCacho Navas, Cristina
dc.contributor.authorReglero Real, Natalia
dc.contributor.authorColás Algora, Natalia
dc.contributor.authorBarroso, Susana
dc.contributor.authorde Rivas, Gema
dc.contributor.authorStamatakis Andriani, Konstantinos 
dc.contributor.authorFeito, Jorge
dc.contributor.authorAndrés, Germán
dc.contributor.authorFresno Escudero, Manuel 
dc.contributor.authorKremer, Leonor
dc.contributor.authorCorreas Hornero, María Isabel 
dc.contributor.authorAlonso, Miguel Angel
dc.contributor.authorMillán, Jaime
dc.contributor.otherUAM. Departamento de Biología Moleculares_ES
dc.date.accessioned2022-10-25T13:14:32Z
dc.date.available2022-10-25T13:14:32Z
dc.date.issued2022-01-09
dc.identifier.citationCellular and Molecular Life Sciences 79.1 (2022): 61es_ES
dc.identifier.issn1420-682X (print)es_ES
dc.identifier.issn1420-9071 (online)es_ES
dc.identifier.urihttp://hdl.handle.net/10486/704746
dc.description.abstractApical localization of Intercellular Adhesion Receptor (ICAM)-1 regulates the adhesion and guidance of leukocytes across polarized epithelial barriers. Here, we investigate the molecular mechanisms that determine ICAM-1 localization into apical membrane domains of polarized hepatic epithelial cells, and their effect on lymphocyte-hepatic epithelial cell interaction. We had previously shown that segregation of ICAM-1 into apical membrane domains, which form bile canaliculi and bile ducts in hepatic epithelial cells, requires basolateral-to-apical transcytosis. Searching for protein machinery potentially involved in ICAM-1 polarization we found that the SNARE-associated protein plasmolipin (PLLP) is expressed in the subapical compartment of hepatic epithelial cells in vitro and in vivo. BioID analysis of ICAM-1 revealed proximal interaction between this adhesion receptor and PLLP. ICAM-1 colocalized and interacted with PLLP during the transcytosis of the receptor. PLLP gene editing and silencing increased the basolateral localization and reduced the apical confinement of ICAM-1 without affecting apicobasal polarity of hepatic epithelial cells, indicating that ICAM-1 transcytosis is specifically impaired in the absence of PLLP. Importantly, PLLP depletion was sufficient to increase T-cell adhesion to hepatic epithelial cells. Such an increase depended on the epithelial cell polarity and ICAM-1 expression, showing that the epithelial transcytotic machinery regulates the adhesion of lymphocytes to polarized epithelial cells. Our findings strongly suggest that the polarized intracellular transport of adhesion receptors constitutes a new regulatory layer of the epithelial inflammatory responsees_ES
dc.format.extent19 pag.es_ES
dc.format.mimetypeapplication/pdfes_ES
dc.language.isoenges_ES
dc.publisherSpringeres_ES
dc.relation.ispartofCellular and Molecular Life Scienceses_ES
dc.rights© The Author(s) 2022es_ES
dc.subject.otherApicobasal polarityes_ES
dc.subject.otherBioIDes_ES
dc.subject.otherHepatocytees_ES
dc.subject.otherICAM-1es_ES
dc.subject.otherLymphocyte adhesiones_ES
dc.subject.otherPLLPes_ES
dc.subject.otherSubapical compartment, bile canaliculuses_ES
dc.subject.otherTranscytosises_ES
dc.titlePlasmolipin regulates basolateral-to-apical transcytosis of ICAM-1 and leukocyte adhesion in polarized hepatic epithelial cellses_ES
dc.typearticlees_ES
dc.subject.ecienciaBiología y Biomedicina / Biologíaes_ES
dc.relation.publisherversionhttps://doi.org/10.1007/s00018-021-04095-zes_ES
dc.identifier.doi10.1007/s00018-021-04095-zes_ES
dc.identifier.publicationfirstpage1es_ES
dc.identifier.publicationissue1es_ES
dc.identifier.publicationlastpage19es_ES
dc.identifier.publicationvolume79es_ES
dc.relation.projectIDGobierno de España. SAF2017-88187-Res_ES
dc.relation.projectIDGobierno de España. PID2020-119881RB-I00es_ES
dc.relation.projectIDComunidad de Madrid. S2017/BMD-3817/TomoXliveres_ES
dc.relation.projectIDComunidad de Madrid. IND2019/BMD-17139es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/EC/FP7/608765es_ES
dc.type.versioninfo:eu-repo/semantics/publishedVersiones_ES
dc.rights.ccReconocimientoes_ES
dc.rights.accessRightsopenAccesses_ES
dc.facultadUAMFacultad de Cienciases_ES
dc.institutoUAMCentro de Biología Molecular Severo Ochoa (CBMSO)es_ES


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