Free Fatty Acid Receptor 1 Signaling Contributes to Migration, MMP-9 Activity, and Expression of IL-8 Induced by Linoleic Acid in HaCaT Cells

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datacite.alternateIdentifier.citationFrontiers in Pharmacology, 11, 2020
datacite.alternateIdentifier.doi10.3389/fphar.2020.00595
datacite.alternateIdentifier.issn1663-9812
datacite.creatorManosalva, Carolina
datacite.creatorAlarcón, Pablo
datacite.creatorGonzález, Karina
datacite.creatorSoto, Jorge
datacite.creatorIgor, Karin
datacite.creatorPeña, Fernanda
datacite.creatorMedina, Gustavo A.
datacite.creatorBurgos, Rafael Agustín Gustín
datacite.creatorHidalgo, María Angélica
datacite.date2020
datacite.rightsAcceso abierto
datacite.subjectFree Fatty Acids Receptor 1
datacite.subjectInterleukin-8
datacite.subjectKeratinocytes (hacat)
datacite.subjectLinoleic Acid
datacite.subjectMatrix Metalloproteinase-9
datacite.subjectMigration
datacite.subjectNeutrophils
datacite.subjectGelatinase B
datacite.subjectInterleukin 8
datacite.subjectLinoleic Acid
datacite.subjectMitogen Activated Protein Kinase 1
datacite.subjectG Protein Coupled Receptor 40
datacite.subjectGelatinase B
datacite.subjectInterleukin 8
datacite.subjectLinoleic Acid
datacite.subjectMitogen Activated Protein Kinase 1
datacite.subjectMitogen Activated Protein Kinase P38
datacite.subjectArticle
datacite.subjectCalcium Cell Level
datacite.subjectCell Isolation
datacite.subjectCell Migration
datacite.subjectCell Viability Assay
datacite.subjectControlled Study
datacite.subjectCytokine Release
datacite.subjectEnzyme Activation
datacite.subjectHacat Cell Line
datacite.subjectHuman
datacite.subjectHuman Cell
datacite.subjectImmunoblotting
datacite.subjectNeutrophil Chemotaxis
datacite.subjectProtein Expression
datacite.subjectProtein Function
datacite.subjectProtein Phosphorylation
datacite.subjectQuantitative Analysis
datacite.subjectReal Time Polymerase Chain Reaction
datacite.subjectSignal Transduction
datacite.subjectWound Healing
datacite.titleFree Fatty Acid Receptor 1 Signaling Contributes to Migration, MMP-9 Activity, and Expression of IL-8 Induced by Linoleic Acid in HaCaT Cells
dc.date.accessioned2025-10-06T14:21:53Z
dc.date.available2025-10-06T14:21:53Z
dc.description.abstractKeratinocytes and neutrophils are the main cellular components in wound healing during re-epithelization and inflammation. Free fatty acids such as linoleic acid (LA) present beneficial properties for wound healing by modulating the inflammatory response. LA is a natural ligand of free fatty acids receptor 1 (FFA1), a G protein-coupled receptor (GPCR), able to modulate inflammatory process; however, the role of FFA1 in keratinocytes and wound healing remains poorly understood. In this study, we investigated the role of FFA1 signaling in migration, matrix metalloproteinase-9 (MMP-9) activity, and IL-8 expression induced by LA in keratinocytes. We confirmed that HaCaT cells, a human keratinocyte cell line, expresses the FFA1 receptor and GW1100, a selective antagonist of FFA1, decreased LA-induced migration of HaCaT cells. Also, GW9508, a synthetic agonist of FFA1, increased migration of these cells. Furthermore, ERK1/2 and p38 MAPK inhibitors abolished the LA-induced increase in cell migration. Besides, HaCaT cells stimulated with LA or GW9508 increased the activity of MMP-9 and the expression of IL-8. GW1100 partially inhibited both responses. We further evaluated the effects of HaCaT cells conditioned media stimulated with LA or GW9508 on neutrophil chemotaxis. Conditioned media induced neutrophil chemotaxis. Furthermore, IL-8 secreted by HaCaT cells stimulated with LA or GW9508, contributed to neutrophil chemotaxis. In conclusion, LA increased migration, MMP-9 activity, and expression of IL-8 from HaCaT cells via FFA1. Hence, these results showed that the effects induced by LA in keratinocytes can be mediated through FFA1, thus explaining a possible mechanism by which this fatty acid could accelerate wound healing. © 2020 Elsevier B.V., All rights reserved.
dc.description.ia_keywordcells, hacat, migration, induced, keratinocytes, wound, healing
dc.formatPDF
dc.identifier.urihttps://repositoriodigital.uct.cl/handle/10925/6852
dc.language.isoen
dc.publisherFrontiers Media
dc.relationinstname: ANID
dc.relationreponame: Repositorio Digital RI2.0
dc.rights.driverinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/
dc.sourceFrontiers in Pharmacology
dc.subject.ia_oecd1nCiencias Naturales
dc.subject.ia_oecd2nCiencias Biológicas
dc.subject.ia_oecd3nBiología General
dc.type.driverinfo:eu-repo/semantics/article
dc.type.driverhttp://purl.org/coar/resource_type/c_2df8fbb1
dc.type.openaireinfo:eu-repo/semantics/publishedVersion
dspace.entity.typePublication
oaire.citationEdition2020
oaire.citationTitleFrontiers in Pharmacology
oaire.citationVolume11
oaire.fundingReferenceUniversidad Austral de Chile DID-UACH S-2014-13, S-2016-07
oaire.fundingReferenceANID FONDECYT 3170775 (Postdoctorado), 1151047 (Regular)
oaire.licenseConditionObra bajo licencia Creative Commons Atribución 4.0 Internacional
oaire.licenseCondition.urihttps://creativecommons.org/licenses/by/4.0/
oaire.resourceTypeArtículo
oaire.resourceType.enArticle
uct.catalogadorjvu
uct.comunidadCiencias de la Saluden_US
uct.departamentoDepartamento de Procesos Diagnósticos y Evaluación
uct.facultadFacultad de Ciencias de la Salud
uct.indizacionScience Citation Index Expanded - SCIE
uct.indizacionSCOPUS
uct.indizacionWOS
uct.indizacionDOAJ
uct.indizacionPubMed
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