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dc.contributor.authorHåversen, Liliana
dc.contributor.authorSundelin, Jeanna Perman
dc.contributor.authorMardinoglu, Adil
dc.contributor.authorRutberg, Mikael
dc.contributor.authorStåhlman, Marcus
dc.contributor.authorWilhelmsson, Ulrika
dc.contributor.authorHultén, Lillemor Mattsson
dc.contributor.authorPekny, Milos
dc.contributor.authorFogelstrand, Per
dc.contributor.authorBentzon, Jacob F 
dc.contributor.authorLevin, Malin
dc.contributor.authorBorén, Jan
dc.date.accessioned2019-02-07T13:24:05Z
dc.date.available2019-02-07T13:24:05Z
dc.date.issued2018-11-19
dc.identifier.citationSci Rep. 2018; 8(1):16973es_ES
dc.identifier.issn2045-2322es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/7140
dc.description.abstractThe aim was to clarify the role of vimentin, an intermediate filament protein abundantly expressed in activated macrophages and foam cells, in macrophages during atherogenesis. Global gene expression, lipid uptake, ROS, and inflammation were analyzed in bone-marrow derived macrophages from vimentin-deficient (Vim-/-) and wild-type (Vim+/+) mice. Atherosclerosis was induced in Ldlr-/- mice transplanted with Vim-/- and Vim+/+ bone marrow, and in Vim-/- and Vim+/+ mice injected with a PCSK9 gain-of-function virus. The mice were fed an atherogenic diet for 12-15 weeks. We observed impaired uptake of native LDL but increased uptake of oxLDL in Vim-/- macrophages. FACS analysis revealed increased surface expression of the scavenger receptor CD36 on Vim-/- macrophages. Vim-/- macrophages also displayed increased markers of oxidative stress, activity of the transcription factor NF-κB, secretion of proinflammatory cytokines and GLUT1-mediated glucose uptake. Vim-/- mice displayed decreased atherogenesis despite increased vascular inflammation and increased CD36 expression on macrophages in two mouse models of atherosclerosis. We demonstrate that vimentin has a strong suppressive effect on oxidative stress and that Vim-/- mice display increased vascular inflammation with increased CD36 expression on macrophages despite decreased subendothelial lipid accumulation. Thus, vimentin has a key role in regulating inflammation in macrophages during atherogenesis.es_ES
dc.description.sponsorshipThis work was supported by the Swedish Research Council, the Swedish Heart-Lung Foundation, and the Sahlgrenska University Hospital ALF research grants.es_ES
dc.language.isoenges_ES
dc.publisherNature Publishing Groupes_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.titleVimentin deficiency in macrophages induces increased oxidative stress and vascular inflammation but attenuates atherosclerosis in micees_ES
dc.typeArtículoes_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID30451917es_ES
dc.format.volume8es_ES
dc.format.number1es_ES
dc.format.page16973es_ES
dc.identifier.doi10.1038/s41598-018-34659-2es_ES
dc.contributor.funderSwedish Research Council
dc.contributor.funderSwedish Heart-Lung Foundation
dc.description.peerreviewedes_ES
dc.identifier.e-issn2045-2322es_ES
dc.relation.publisherversionhttps://doi.org/10.1038/s41598-018-34659-2es_ES
dc.identifier.journalScientific reportses_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Patología Experimental de la Aterosclerosises_ES
dc.repisalud.institucionCNICes_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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Atribución 4.0 Internacional
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