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Authordc.contributor.authorOlivares Silva, Francisco Javier 
Authordc.contributor.authorLandaeta, Rodolfo 
Authordc.contributor.authorAránguiz, Pablo 
Authordc.contributor.authorBolivar, Samir 
Authordc.contributor.authorHumeres Martínez, Claudio 
Authordc.contributor.authorAnfossi, Renatto 
Authordc.contributor.authorVivar Sánchez, Raúl 
Authordc.contributor.authorBoza Fuentes, Pía 
Authordc.contributor.authorMuñoz Jofré, Claudia 
Authordc.contributor.authorPardo Jiménez, Viviana Gladys 
Authordc.contributor.authorPeiro, Concepción 
Authordc.contributor.authorSánchez Ferrer, Carlos 
Authordc.contributor.authorDíaz Araya, Guillermo 
Admission datedc.date.accessioned2018-07-30T15:43:56Z
Available datedc.date.available2018-07-30T15:43:56Z
Publication datedc.date.issued2018
Cita de ítemdc.identifier.citationBBA - Molecular Basis of Disease, 1864 (2018): 831–842es_ES
Identifierdc.identifier.other10.1016/j.bbadis.2017.12.002
Identifierdc.identifier.urihttps://repositorio.uchile.cl/handle/2250/150425
Abstractdc.description.abstractCardiac fibroblasts (CF) act as sentinel cells responding to chemokines, cytokines and growth factors released in cardiac tissue in cardiac injury events, such as myocardial infarction (MI). Cardiac injury involves the release of various damage-associated molecular patterns (DAMPs) including heparan sulfate (HS), a constituent of the extracellular matrix (ECM), through the TLR4 receptor activation triggering a strong inflammatory response, inducing leukocytes recruitment. This latter cells are responsible of clearing cell debris and releasing cytokines that promote CF differentiation to myofibroblast (CMF), thus initiating scar formation. CF were isolated from adult male rats and subsequently stimulated with HS or LPS, in the presence or absence of chemical inhibitors, to evaluate signaling pathways involved in ICAM-1 and VCAM-1 expression. siRNA against ICAM-1 and VCAM-1 were used to evaluate participation of these adhesion molecules on leukocytes recruitment. HS through TLR4, PI3K/Ala and NF-KB increased ICAM-1 and VCAM-1 expression, which favored the adhesion of spleen mononuclear cells (SMC) and bone marrow granulocytes (PMN) to CF. These effects were prevented by siRNA against ICAM-1 and VCAM-1. Co-culture of CF with SMC increased alpha-SMA expression, skewing CF towards a pro-fibrotic phenotype, while CF pretreatment with HS partially reverted this effect. Conclusion: These data show the dual role of HS during the initial stages of wound healing. Initially, HS enhance the pro-inflammatory role of CF increasing cytokines secretion; and later, by increasing protein adhesion molecules allows the adhesion of SMC on CF, which trigger CF-to-CMF differentiation.es_ES
Patrocinadordc.description.sponsorshipFONDECYT 1170425 FONDAP ACCDiS 15130011 CEAL-AL/2017-022es_ES
Lenguagedc.language.isoenes_ES
Publisherdc.publisherElsevieres_ES
Type of licensedc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile*
Link to Licensedc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/*
Sourcedc.sourceBBA - Molecular Basis of Diseasees_ES
Keywordsdc.subjectCardiac fibroblastes_ES
Keywordsdc.subjectHeparan sulfatees_ES
Keywordsdc.subjectLeukocytees_ES
Keywordsdc.subjectTLR4es_ES
Keywordsdc.subjectalpha-SMAes_ES
Títulodc.titleHeparan sulfate potentiates leukocyte adhesion on cardiac fibroblast by enhancing Vcam-1 and Icam-1 expressiones_ES
Document typedc.typeArtículo de revista
Catalogueruchile.catalogadortjnes_ES
Indexationuchile.indexArtículo de publicación ISIes_ES


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Attribution-NonCommercial-NoDerivs 3.0 Chile
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs 3.0 Chile