Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/75027
Title: Fcγ Receptor Deficiency Attenuates Diabetic Nephropathy
Authors: Lopez-Parra, Virginia
Mallavia, Beñat
Lopez-Franco, Oscar
Ortiz-Muñoz, Guadalupe
Oguiza, Ainhoa
Recio Cruz, Carlota Pilar 
Blanco, Julia
Nimmerjahn, Falk
Egido, Jesus
Gómez-Guerrero, Carmen
UNESCO Clasification: 3207 Patología
320506 Nefrología
Issue Date: 2012
Project: SAF2009/11794
PI10/00072
RECAVA RD06/0014/0035
Journal: Journal of the American Society of Nephrology : JASN 
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.
URI: http://hdl.handle.net/10553/75027
ISSN: 1046-6673
DOI: 10.1681/ASN.2011080822
Source: Journal of the American Society of Nephrology : JASN [ISSN 1046-6673], v. 23 (9), p. 1518-1527
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