Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/75286
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dc.contributor.authorMallavia, Beñaten_US
dc.contributor.authorOguiza, Ainhoaen_US
dc.contributor.authorLopez-Franco, Oscaren_US
dc.contributor.authorRecio Cruz, Carlota Pilaren_US
dc.contributor.authorOrtiz-Muñoz, Guadalupeen_US
dc.contributor.authorLazaro, Iolandaen_US
dc.contributor.authorLopez-Parra, Virginiaen_US
dc.contributor.authorEgido, Jesusen_US
dc.contributor.authorGomez-Guerrero, Carmenen_US
dc.contributor.editorLutgens, Esther-
dc.date.accessioned2020-11-09T16:38:08Z-
dc.date.available2020-11-09T16:38:08Z-
dc.date.issued2013en_US
dc.identifier.issn1932-6203en_US
dc.identifier.urihttp://hdl.handle.net/10553/75286-
dc.description.abstractImmunity contributes to arterial inflammation during atherosclerosis. Oxidized low-density lipoproteins induce an autoimmune response characterized by specific antibodies and immune complexes in atherosclerotic patients. We hypothesize that specific Fcγ receptors for IgG constant region participate in atherogenesis by regulating the inflammatory state of lesional macrophages. In vivo we examined the role of activating Fcγ receptors in atherosclerosis progression using bone marrow transplantation from mice deficient in γ-chain (the common signaling subunit of activating Fcγ receptors) to hyperlipidemic mice. Hematopoietic deficiency of Fcγ receptors significantly reduced atherosclerotic lesion size, which was associated with decreased number of macrophages and T lymphocytes, and increased T regulatory cell function. Lesions of Fcγ receptor deficient mice exhibited increased plaque stability, as evidenced by higher collagen and smooth muscle cell content and decreased apoptosis. These effects were independent of changes in serum lipids and antibody response to oxidized low-density lipoproteins. Activating Fcγ receptor deficiency reduced pro-inflammatory gene expression, nuclear factor-κB activity, and M1 macrophages at the lesion site, while increasing anti-inflammatory genes and M2 macrophages. The decreased inflammation in the lesions was mirrored by a reduced number of classical inflammatory monocytes in blood. In vitro, lack of activating Fcγ receptors attenuated foam cell formation, oxidative stress and pro-inflammatory gene expression, and increased M2-associated genes in murine macrophages. Our study demonstrates that activating Fcγ receptors influence the macrophage phenotypic balance in the artery wall of atherosclerotic mice and suggests that modulation of Fcγ receptor-mediated inflammatory responses could effectively suppress atherosclerosis.en_US
dc.languageengen_US
dc.relationSAF2009-11794en_US
dc.relationSAF2012-38830en_US
dc.relationFIS PI10/00072en_US
dc.relationRECAVA RD12/0042/0038en_US
dc.relation.ispartofPLoS ONEen_US
dc.sourcePLoS ONE [ISSN 1932-6203], v. 8 (6), e66754en_US
dc.subject3207 Patologíaen_US
dc.titleGene Deficiency in Activating Fcγ Receptors Influences the Macrophage Phenotypic Balance and Reduces Atherosclerosis in Miceen_US
dc.typeinfo:eu-repo/semantics/articleen_US
dc.typeArticleen_US
dc.identifier.doi10.1371/journal.pone.0066754en_US
dc.identifier.issue6-
dc.investigacionCiencias de la Saluden_US
dc.type2Artículoen_US
dc.utils.revisionen_US
dc.contributor.wosstandardLutgens, Esther-
dc.contributor.wosstandardLutgens, Esther-
dc.identifier.ulpgcNoen_US
dc.contributor.buulpgcBU-MEDen_US
dc.description.sjr1,74
dc.description.jcr3,534
dc.description.sjrqQ1
dc.description.jcrqQ1
dc.description.scieSCIE
dc.description.erihplusERIH PLUS
item.grantfulltextopen-
item.fulltextCon texto completo-
crisitem.author.deptGIR IUIBS: Farmacología Molecular y Traslacional-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.orcid0000-0002-8832-2826-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.fullNameRecio Cruz, Carlota Pilar-
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