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Authordc.contributor.authorDi Summa, Francesca 
Authordc.contributor.authorKargarpour, Zahra 
Authordc.contributor.authorNasirzade, Jila 
Authordc.contributor.authorStähli, Alexandra 
Authordc.contributor.authorMitulović, Goran 
Authordc.contributor.authorPanić Janković, Tanja 
Authordc.contributor.authorKoller, Veronika 
Authordc.contributor.authorKaltenbach, Cosima 
Authordc.contributor.authorMüller, Heinz 
Authordc.contributor.authorPanahipour, Layla 
Authordc.contributor.authorGruber, Reinhard 
Authordc.contributor.authorStrauss, Franz Josef 
Admission datedc.date.accessioned2020-08-24T20:21:03Z
Available datedc.date.available2020-08-24T20:21:03Z
Publication datedc.date.issued2020
Cita de ítemdc.identifier.citationScientific Reports 10(1): 2020es_ES
Identifierdc.identifier.other10.1038/s41598-020-67167-3
Identifierdc.identifier.urihttps://repositorio.uchile.cl/handle/2250/176541
Abstractdc.description.abstractPlatelet-rich fibrin (PRF) contains a broad spectrum of bioactive molecules that can trigger several cellular responses. However, these molecules along with their upstream responses remain mostly uninvestigated. By means of proteomics we revealed that PRF lysates contain more than 650 proteins, being TGF-beta one of the few growth factors found. To uncover the major target genes regulated by PRF lysates, gingival fibroblasts were exposed to lysates obtained from PRF membranes followed by a whole genome array. We identified 51 genes strongly regulated by PRF including IL11, NOX4 and PRG4 which are characteristic TGF-beta target genes. RT-PCR and immunoassay analysis confirmed the TGF-beta receptor I kinase-dependent increased expression of IL11, NOX4 and PRG4. The PRF-derived TGF-beta activity was verified by the translocation of Smad2/3 into the nucleus along with the increased phosphorylation of Smad3. Considering that PRF is clinically used in combination with dental implants and collagen membranes, we showed here that PRF-derived TGF-beta activity adsorbs to titanium implants and collagen membranes indicated by the changes in gene expression and immunoassay analysis. Our study points towards TGF-beta as major target of PRF and suggest that TGF-beta activity released by PRF adsorbs to titanium surface and collagen membraneses_ES
Patrocinadordc.description.sponsorshipOsteology Foundation, Switzerland 17-125 14-126 Austrian Science Fund (FWF) 4072-B28 Comisión Nacional de Investigación Científica y Tecnológica (CONICYT) Osteology Foundationes_ES
Lenguagedc.language.isoenes_ES
Publisherdc.publisherNaturees_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.sourceScientific Reportses_ES
Keywordsdc.subjectGene-expressiones_ES
Keywordsdc.subjectGrowth-factorses_ES
Keywordsdc.subjectRidge preservationes_ES
Keywordsdc.subjectBone defectses_ES
Keywordsdc.subjectCellses_ES
Keywordsdc.subjectDifferentiationes_ES
Keywordsdc.subjectOsteoblastes_ES
Keywordsdc.subjectInterleukin-11es_ES
Keywordsdc.subjectLeukocytees_ES
Keywordsdc.subjectPRFes_ES
Títulodc.titleTGFβ activity released from platelet-rich fibrin adsorbs to titanium surface and collagen membraneses_ES
Document typedc.typeArtículo de revistaes_ES
dcterms.accessRightsdcterms.accessRightsAcceso Abierto
Catalogueruchile.catalogadorctces_ES
Indexationuchile.indexArtículo de publicación ISI
Indexationuchile.indexArtículo de publicación SCOPUS


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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