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Use este identificador para citar o ir al link de este elemento: http://hdl.handle.net/1843/53961
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Campo DCValorIdioma
dc.creatorMarina Chaves de Oliveirapt_BR
dc.creatorBartijn Pieterspt_BR
dc.creatorPolianna B. Guimarãespt_BR
dc.creatorLetícia F. Dufflespt_BR
dc.creatorJoyce Elisa Herediapt_BR
dc.creatorAna Letícia Malheiros Silveirapt_BR
dc.creatorAmanda C. C. Oliveirapt_BR
dc.creatorMauro Martins Teixeirapt_BR
dc.creatorAdaliene Versiani Matos Ferreirapt_BR
dc.creatorTarcilia A Silvapt_BR
dc.creatorFons Van De Loopt_BR
dc.creatorSoraia Macaript_BR
dc.date.accessioned2023-05-25T20:15:57Z-
dc.date.available2023-05-25T20:15:57Z-
dc.date.issued2020-
dc.citation.volume8pt_BR
dc.identifier.doihttps://doi.org/10.3389/fbioe.2020.00891pt_BR
dc.identifier.issn2296-4185pt_BR
dc.identifier.urihttp://hdl.handle.net/1843/53961-
dc.description.resumoStudying effects of milk components on bone may have a clinical impact as milk is highly associated with bone maintenance, and clinical studies provided controversial associations with dairy consumption. We aimed to evaluate the impact of milk extracellular vesicles (mEVs) on the dynamics of bone loss in mice. MEVs are nanoparticles containing proteins, mRNA and microRNA, and were supplemented into the drinking water of mice, either receiving diet-induced obesity or ovariectomy (OVX). Mice receiving mEVs were protected from the bone loss caused by diet-induced obesity. In a more severe model of bone loss, OVX, higher osteoclast numbers in the femur were found, which were lowered by mEV treatment. Additionally, the osteoclastogenic potential of bone marrow-derived precursor cells was lowered in mEV-treated mice. The reduced stiffness in the femur of OVX mice was consequently reversed by mEV treatment, accompanied by improvement in the bone microarchitecture. In general, the RANKL/OPG ratio increased systemically and locally in both models and was rescued by mEV treatment. The number of osteocytes, as primary regulators of the RANKL/OPG system, raised in the femur of the OVX mEVs-treated group compared to OVX nontreated mice. Also, the osteocyte cell line treated with mEVs demonstrated a lowered RANKL/OPG ratio. Thus, mEVs showed systemic and local osteoprotective properties in two mouse models of bone loss reflected in reduced osteoclast presence. Data reveal mEV potential in bone modulation, acting via osteocyte enhancement and RANKL/OPG regulation. We suggest that mEVs could be a therapeutic candidate for the treatment of bone loss.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.languageporpt_BR
dc.publisherUniversidade Federal de Minas Geraispt_BR
dc.publisher.countryBrasilpt_BR
dc.publisher.departmentENF - DEPARTAMENTO DE NUTRIÇÃOpt_BR
dc.publisher.departmentFAO - DEPARTAMENTO DE ODONTOLOGIA RESTAURADORApt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE BIOQUÍMICA E IMUNOLOGIApt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE FARMACOLOGIApt_BR
dc.publisher.initialsUFMGpt_BR
dc.relation.ispartofFrontiers in bioengineering and biotechnologypt_BR
dc.rightsAcesso Abertopt_BR
dc.subjectextracellular vesiclespt_BR
dc.subjectmilkpt_BR
dc.subjectbone losspt_BR
dc.subjectosteoporosispt_BR
dc.subjectobesitypt_BR
dc.subjectosteocytept_BR
dc.subject.otherVesículas extracelularespt_BR
dc.subject.otherLeitept_BR
dc.subject.otherOsteoporosept_BR
dc.subject.otherObesidadept_BR
dc.subject.otherOsteócitospt_BR
dc.titleBovine milk extracellular vesicles are osteoprotective by increasing osteocyte numbers and targeting RANKL/OPG system in experimental models of bone losspt_BR
dc.typeArtigo de Periódicopt_BR
dc.url.externahttps://www.frontiersin.org/articles/10.3389/fbioe.2020.00891/fullpt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-7423-9802pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-7171-3145pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-2839-8757pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-1052-0854pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-6944-3008pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-2256-8652pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-5851-099Xpt_BR
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