Fcγ receptor deficiency attenuates diabetic nephropathy

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dc.contributor.author López-Parra, Virginia
dc.contributor.author Mallavia, Beñat
dc.contributor.author López-Franco, Óscar
dc.contributor.author Ortiz-Muñoz, Guadalupe
dc.contributor.author Oguiza, Ainhoa
dc.contributor.author Recio, Carlota
dc.contributor.author Blanco, Julia A Parra
dc.contributor.author Nimmerjahn, F.
dc.contributor.author Egido de los Ríos, Jesús
dc.contributor.author Gómez-Guerrero, Carmen
dc.contributor.other UAM. Departamento de Medicina es_ES
dc.date.accessioned 2015-05-20T11:54:19Z
dc.date.available 2015-05-20T11:54:19Z
dc.date.issued 2012-09-01
dc.identifier.citation Journal of the American Society of Nephrology 23.9 (2012): 1518–1527 en_US
dc.identifier.issn 1046-6673 (print) en_US
dc.identifier.issn 2309-1518 (online) en_US
dc.identifier.uri http://hdl.handle.net/10486/666271
dc.description.abstract Among patients with diabetes, increased production of immunoglobulins against proteins modified by diabetes is associated with proteinuria and cardiovascular risk, suggesting that immune mechanisms may contribute to the development of diabetes complications, such as nephropathy. We investigated the contribution of IgG Fcg receptors to diabetic renal injury in hyperglycemic, hypercholesterolemic mice. Weused streptozotocin to induce diabetes in apolipoprotein E–deficientmice and in mice deficient in both apolipoprotein E and g-chain, the common subunit of activating Fcg receptors. After 15 weeks, the mice lacking Fcg receptors had significantly less albuminuria and renal hypertrophy, despite similar degrees of hyperglycemia and hypercholesterolemia, immunoglobulin production, and glomerular immune deposits. Moreover, diabetic Fcg receptor–deficient mice had less mesangial matrix expansion, inflammatory cell infiltration, and collagen and a-smooth muscle actin content in their kidneys. Accordingly, expression of genes involved in leukocyte infiltration, fibrosis, and oxidative stress was significantly reduced in diabetic kidneys and in mesangial cells cultured from Fcg receptor–deficient mice. In summary, preventing the activation of Fcg receptors alleviates renal hypertrophy, inflammation, and fibrosis in hypercholesterolemic mice with diabetes, suggesting that modulating Fcg receptor signaling may be renoprotective in diabetic nephropathy en_US
dc.description.sponsorship This study was supported by grants from Spanish Ministry of Science (SAF2009/11794), Ministry of Health (PI10/00072, RECAVA RD06/0014/0035), Lilly Foundation, FRIAT, and Spanish Society of Nephrology es_ES
dc.format.extent 10 pag. en
dc.format.mimetype application/pdf en
dc.language.iso eng en
dc.publisher American Society of Nephrology
dc.relation.ispartof Journal of the American Society of Nephrology en_US
dc.rights © 2012 by the American Society of Nephrology en_US
dc.subject.other Albuminuria es_ES
dc.subject.other Diabetes Mellitus en_US
dc.subject.other Diabetic Nephropathies en_US
dc.subject.other Hypertrophy en_US
dc.title Fcγ receptor deficiency attenuates diabetic nephropathy en_US
dc.type article en
dc.subject.eciencia Medicina es_ES
dc.relation.publisherversion http://dx.doi.org/10.1681/ASN.2011080822 es_ES
dc.identifier.doi 10.1681/ASN.2011080822 es_ES
dc.identifier.publicationfirstpage 1518 es_ES
dc.identifier.publicationissue 9 es_ES
dc.identifier.publicationlastpage 1527 es_ES
dc.identifier.publicationvolume 23 es_ES
dc.type.version info:eu-repo/semantics/publishedVersion en
dc.rights.accessRights openAccess en
dc.authorUAM Egido De Los Ríos, Jesús (259718)

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