Fcγ Receptor Deficiency Confers Protection Against Atherosclerosis in Apolipoprotein E Knockout Mice

IgG Fc receptors (FcγRs) play a role in activating the immune system and in maintaining peripheral tolerance, but their role in atherosclerosis is unknown. We generated double-knockout (DKO) mice by crossing apolipoprotein E–deficient mice (apoE−/−) with FcγR γ chain–deficient mice (γ−/−). The size...

Descripción completa

Detalles Bibliográficos
Autores: Hernández-Vargas, Purificación, Ortiz-Muñoz, Guadalupe, López-Franco, Oscar, Suzuki, Yusuke, Gallego-Delgado, Julio, Sanjuán, Guillermo, Lázaro, Alberto, López-Parra, Virginia, Ortega, Luis, Egido, Jesús, Gómez-Guerrero, Carmen
Tipo de recurso: artículo
Estado:Versión enviada para evaluación y publicación
Fecha de publicación:2006
País:España
Institución:Consejo Superior de Investigaciones Científicas (CSIC)
Repositorio:DIGITAL.CSIC. Repositorio Institucional del CSIC
OAI Identifier:oai:digital.csic.es:10261/378095
Acceso en línea:http://hdl.handle.net/10261/378095
Access Level:acceso abierto
Palabra clave:Fc receptors
Atherosclerosis
Double-knockout mice
Immune complexes
id ES_6baebee9a1a744622cdeffb14d64b170
oai_identifier_str oai:digital.csic.es:10261/378095
network_acronym_str ES
network_name_str España
repository_id_str
spelling Fcγ Receptor Deficiency Confers Protection Against Atherosclerosis in Apolipoprotein E Knockout MiceHernández-Vargas, PurificaciónOrtiz-Muñoz, GuadalupeLópez-Franco, OscarSuzuki, YusukeGallego-Delgado, JulioSanjuán, GuillermoLázaro, AlbertoLópez-Parra, VirginiaOrtega, LuisEgido, JesúsGómez-Guerrero, CarmenFc receptorsAtherosclerosisDouble-knockout miceImmune complexesIgG Fc receptors (FcγRs) play a role in activating the immune system and in maintaining peripheral tolerance, but their role in atherosclerosis is unknown. We generated double-knockout (DKO) mice by crossing apolipoprotein E–deficient mice (apoE−/−) with FcγR γ chain–deficient mice (γ−/−). The size of atherosclerotic lesions along the aorta was approximately 50% lower in DKO compared with apoE−/− control mice, without differences in serum lipid levels. The macrophage and T-cell content of lesions in the DKO were reduced by 49±6% and 56±8%, respectively, compared with the content in apoE−/− lesions. Furthermore, the expression of monocyte chemoattractant protein-1 (MCP-1), RANTES (Regulated on Activated Normal T-cell Expressed and Secreted), and intercellular adhesion molecule-1 (ICAM-1) and the activation of nuclear factor-κB (NF-κB) were significantly reduced in aortic lesions from DKO mice. In vitro, vascular smooth muscle cells (VSMCs) from both γ−/− and DKO mice failed to respond to immune complexes, as shown by impaired chemokine expression and NF-κB activation. ApoE−/− mice have higher levels of activating FcγRI and FcγRIIIA, and inhibitory FcγRIIB, compared with wild-type mice. The DKO mice express only the inhibitory FcγRIIB receptor. We conclude that FcγR deficiency limits development and progression of atherosclerosis. In addition to leukocytes, FcγR activation in VSMCs contributes to the inflammatory process, in part, by regulating chemokine expression and leukocyte invasion of the vessel wall. These results underscore the critical role of FcγRs in atherogenesis and support the use of immunotherapy in the treatment of this disease.This work was supported by grants from the Fondo de Investigacion Sanitaria (PI02/0539), Comunidad Autónoma de Madrid (GR/SAL/0411/2004), Ministerio de Educación y Cultura (2005/05857; and Ramon y Cajal Program to C.G.-G.), and Mutua Madrileña. G.O.-M. and V.L.-P. are fellows from Fondo de Investigacion Sanitaria and Comunidad Autónoma de Madrid, respectively.NoAmerican Heart AssociationComunidad de MadridMinisterio de Educación y Cultura (España)Fundación Mutua Madrileña202520252006info:eu-repo/semantics/articlehttp://purl.org/coar/resource_type/c_6501Preprintinfo:eu-repo/semantics/submittedVersionapplication/pdfhttp://hdl.handle.net/10261/378095reponame:DIGITAL.CSIC. Repositorio Institucional del CSICinstname:Consejo Superior de Investigaciones Científicas (CSIC)Ingléshttps://doi.org/10.1161/01.RES.0000250556.07796.6cNoinfo:eu-repo/semantics/openAccessoai:digital.csic.es:10261/3780952026-05-22T06:33:51Z
dc.title.none.fl_str_mv Fcγ Receptor Deficiency Confers Protection Against Atherosclerosis in Apolipoprotein E Knockout Mice
title Fcγ Receptor Deficiency Confers Protection Against Atherosclerosis in Apolipoprotein E Knockout Mice
spellingShingle Fcγ Receptor Deficiency Confers Protection Against Atherosclerosis in Apolipoprotein E Knockout Mice
Hernández-Vargas, Purificación
Fc receptors
Atherosclerosis
Double-knockout mice
Immune complexes
title_short Fcγ Receptor Deficiency Confers Protection Against Atherosclerosis in Apolipoprotein E Knockout Mice
title_full Fcγ Receptor Deficiency Confers Protection Against Atherosclerosis in Apolipoprotein E Knockout Mice
title_fullStr Fcγ Receptor Deficiency Confers Protection Against Atherosclerosis in Apolipoprotein E Knockout Mice
title_full_unstemmed Fcγ Receptor Deficiency Confers Protection Against Atherosclerosis in Apolipoprotein E Knockout Mice
title_sort Fcγ Receptor Deficiency Confers Protection Against Atherosclerosis in Apolipoprotein E Knockout Mice
dc.creator.none.fl_str_mv Hernández-Vargas, Purificación
Ortiz-Muñoz, Guadalupe
López-Franco, Oscar
Suzuki, Yusuke
Gallego-Delgado, Julio
Sanjuán, Guillermo
Lázaro, Alberto
López-Parra, Virginia
Ortega, Luis
Egido, Jesús
Gómez-Guerrero, Carmen
author Hernández-Vargas, Purificación
author_facet Hernández-Vargas, Purificación
Ortiz-Muñoz, Guadalupe
López-Franco, Oscar
Suzuki, Yusuke
Gallego-Delgado, Julio
Sanjuán, Guillermo
Lázaro, Alberto
López-Parra, Virginia
Ortega, Luis
Egido, Jesús
Gómez-Guerrero, Carmen
author_role author
author2 Ortiz-Muñoz, Guadalupe
López-Franco, Oscar
Suzuki, Yusuke
Gallego-Delgado, Julio
Sanjuán, Guillermo
Lázaro, Alberto
López-Parra, Virginia
Ortega, Luis
Egido, Jesús
Gómez-Guerrero, Carmen
author2_role author
author
author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Comunidad de Madrid
Ministerio de Educación y Cultura (España)
Fundación Mutua Madrileña
dc.subject.none.fl_str_mv Fc receptors
Atherosclerosis
Double-knockout mice
Immune complexes
topic Fc receptors
Atherosclerosis
Double-knockout mice
Immune complexes
description IgG Fc receptors (FcγRs) play a role in activating the immune system and in maintaining peripheral tolerance, but their role in atherosclerosis is unknown. We generated double-knockout (DKO) mice by crossing apolipoprotein E–deficient mice (apoE−/−) with FcγR γ chain–deficient mice (γ−/−). The size of atherosclerotic lesions along the aorta was approximately 50% lower in DKO compared with apoE−/− control mice, without differences in serum lipid levels. The macrophage and T-cell content of lesions in the DKO were reduced by 49±6% and 56±8%, respectively, compared with the content in apoE−/− lesions. Furthermore, the expression of monocyte chemoattractant protein-1 (MCP-1), RANTES (Regulated on Activated Normal T-cell Expressed and Secreted), and intercellular adhesion molecule-1 (ICAM-1) and the activation of nuclear factor-κB (NF-κB) were significantly reduced in aortic lesions from DKO mice. In vitro, vascular smooth muscle cells (VSMCs) from both γ−/− and DKO mice failed to respond to immune complexes, as shown by impaired chemokine expression and NF-κB activation. ApoE−/− mice have higher levels of activating FcγRI and FcγRIIIA, and inhibitory FcγRIIB, compared with wild-type mice. The DKO mice express only the inhibitory FcγRIIB receptor. We conclude that FcγR deficiency limits development and progression of atherosclerosis. In addition to leukocytes, FcγR activation in VSMCs contributes to the inflammatory process, in part, by regulating chemokine expression and leukocyte invasion of the vessel wall. These results underscore the critical role of FcγRs in atherogenesis and support the use of immunotherapy in the treatment of this disease.
publishDate 2006
dc.date.none.fl_str_mv 2006
2025
2025
dc.type.none.fl_str_mv info:eu-repo/semantics/article
http://purl.org/coar/resource_type/c_6501
Preprint
info:eu-repo/semantics/submittedVersion
format article
status_str submittedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/10261/378095
url http://hdl.handle.net/10261/378095
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv https://doi.org/10.1161/01.RES.0000250556.07796.6c
No
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv American Heart Association
publisher.none.fl_str_mv American Heart Association
dc.source.none.fl_str_mv reponame:DIGITAL.CSIC. Repositorio Institucional del CSIC
instname:Consejo Superior de Investigaciones Científicas (CSIC)
instname_str Consejo Superior de Investigaciones Científicas (CSIC)
reponame_str DIGITAL.CSIC. Repositorio Institucional del CSIC
collection DIGITAL.CSIC. Repositorio Institucional del CSIC
repository.name.fl_str_mv
repository.mail.fl_str_mv
_version_ 1869410214306906112
score 15,812429