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, Vol. 55, N° 595, 2020en_US
datacite.alternateIdentifier.doi10.3389/fphar.2020.00595en_US
datacite.alternateIdentifier.issn1663-9812 (electrónica)en_US
datacite.creatorManosalva, Carolina
datacite.creatorAlarcón, Pablo
datacite.creatorGonzalez, Karina
datacite.creatorSoto, Jorge
datacite.creatorIgor, Karin
datacite.creatorPeña, Fernanda
datacite.creatorMedina, Gustavo
datacite.creatorBurgos, Rafael
datacite.creatorHidalgo, María A.
datacite.date2020-05
datacite.subjectLinoleic aciden_US
datacite.subjectMigration
datacite.subjectNeutrophils
datacite.subjectKeratinocytes (HaCaT)
datacite.subjectFree fatty acids receptor 1
datacite.subjectInterleukin-8
datacite.subjectMatrix metalloproteinase-9
datacite.titleFree Fatty Acid Receptor 1 Signaling Contributes to Migration, MMP-9 Activity, and Expression of IL-8 Induced by Linoleic Acid in HaCaT Cellsen_US
dc.coverageChileen_US
dc.date.accessioned2024-03-18T19:49:19Z
dc.date.available2024-03-18T19:49:19Z
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.en_US
dc.formatPDFen_US
dc.identifier.urihttps://repositoriodigital.uct.cl/handle/10925/5551
dc.language.isoenen_US
dc.rightsFRONTIERS MEDIA SAen_US
dc.rightsObra bajo licencia Creative Commons Atribucion 4.0 Internacional
dc.sourceRevista Frontiers in Pharmacologyen_US
oaire.resourceTypeArtículo de Revistaen_US
oaire.versionpostprinten_US
uct.carreraTecnología Médicaen_US
uct.catalogadorJCCLen_US
uct.comunidadCiencias de la Saluden_US
uct.facultadFacultad de Ciencias de la Saluden_US
uct.indizacionSCI EXPANDEDen_US
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