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Please use this identifier to cite or link to this item: http://hdl.handle.net/1843/56578
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dc.creatorAndrea da Fonseca Ferreirapt_BR
dc.creatorPricila da Silva Cunhapt_BR
dc.creatorVirgínia Mendes Carregalpt_BR
dc.creatorPriscila de Cássia da Silvapt_BR
dc.creatorMarcelo Coutinho de Mirandapt_BR
dc.creatorMarianna Kunrath-Limapt_BR
dc.creatorMariane Izabella Abreu de Melopt_BR
dc.creatorCamila Cristina Fraga Faracopt_BR
dc.creatorJoana Lobato Barbosapt_BR
dc.creatorFrédéric Frezardpt_BR
dc.creatorVivian Resendept_BR
dc.creatorMichele Angela Rodriguespt_BR
dc.creatorAlfredo Miranda de Goespt_BR
dc.creatorDawidson Assis Gomespt_BR
dc.date.accessioned2023-07-18T16:41:17Z-
dc.date.available2023-07-18T16:41:17Z-
dc.date.issued2017-
dc.citation.volume2017pt_BR
dc.identifier.doihttps://doi.org/10.1155/2017/9841035pt_BR
dc.identifier.issn1687-9678pt_BR
dc.identifier.urihttp://hdl.handle.net/1843/56578-
dc.description.resumoMesenchymal stem/stromal cells (MSCs) are promising tools in cell therapy. They secrete extracellular vesicles (EVs) that carry different classes of molecules that can promote skin repair, but the mechanisms are poorly understood. Skin wound healing is a complex process that requires the activity of several signaling pathways and cell types, including keratinocytes and fibroblasts. In this study, we explored whether adipose tissue MSC-derived EVs could accelerate migration and proliferation of keratinocytes and fibroblasts, activate the AKT pathway, and promote wound healing in vivo. Furthermore, we evaluated if EV effects are miR-205 dependent. We found that MSC EVs had an average diameter of 135 nm. Keratinocytes and fibroblasts exposed to EVs exhibited higher levels of proliferation, migration, and AKT activation. Topical administration of EVs accelerated skin wound closure. Knockdown of miR-205 decreased AKT phosphorylation in fibroblasts and keratinocytes, whereas migration was decreased only in keratinocytes. Moreover, knockdown of miR-205 failed to inhibit AKT phosphorylation in fibroblasts and keratinocytes exposed to EVs. About the mechanism of EV effects, we found that incubation with EVs prevented inhibition of AKT activation by miR-205 knockdown, suggesting that EVs activate AKT independently of miR-205. In conclusion, we demonstrated that EVs are a promising tool for wound healing.pt_BR
dc.description.sponsorshipCNPq - Conselho Nacional de Desenvolvimento Científico e Tecnológicopt_BR
dc.description.sponsorshipFAPEMIG - Fundação de Amparo à Pesquisa do Estado de Minas Geraispt_BR
dc.description.sponsorshipCAPES - Coordenação de Aperfeiçoamento de Pessoal de Nível Superiorpt_BR
dc.format.mimetypepdfpt_BR
dc.languageengpt_BR
dc.publisherUniversidade Federal de Minas Geraispt_BR
dc.publisher.countryBrasilpt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE BIOQUÍMICA E IMUNOLOGIApt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE FISIOLOGIA E BIOFÍSICApt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE MORFOLOGIApt_BR
dc.publisher.departmentMED - DEPARTAMENTO DE CIRURGIApt_BR
dc.publisher.initialsUFMGpt_BR
dc.relation.ispartofStem Cells Internationalpt_BR
dc.rightsAcesso Abertopt_BR
dc.subjectMesenchymal stempt_BR
dc.subjectStromal Cellspt_BR
dc.subjectKeratinocytespt_BR
dc.subjectFibroblastspt_BR
dc.subject.otherCélulas-tronco mesenquimaispt_BR
dc.subject.otherCélulas estromaispt_BR
dc.subject.otherQueratinócitospt_BR
dc.subject.otherFibroblastospt_BR
dc.titleExtracellular vesicles from adipose-derived mesenchymal stem/stromal cells accelerate migration and activate AKT pathway in human keratinocytes and fibroblasts independently of miR-205 activitypt_BR
dc.typeArtigo de Periódicopt_BR
dc.url.externahttps://www.hindawi.com/journals/sci/2017/9841035/pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-4633-313Xpt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-5012-7566pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-1863-4963pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-3783-5717pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-4400-0427pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-0233-7729pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-0262-949Xpt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-7714-991Xpt_BR
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