Fcγ receptor deficiency attenuates diabetic nephropathy
Entity
UAM. Departamento de MedicinaPublisher
American Society of NephrologyDate
2012-09-01Citation
10.1681/ASN.2011080822
Journal of the American Society of Nephrology 23.9 (2012): 1518–1527
ISSN
1046-6673 (print); 2309-1518 (online)DOI
10.1681/ASN.2011080822Funded by
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 NephrologyEditor's Version
http://dx.doi.org/10.1681/ASN.2011080822Subjects
Albuminuria; Diabetes Mellitus; Diabetic Nephropathies; Hypertrophy; MedicinaRights
© 2012 by the American Society of NephrologyAbstract
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
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Google Scholar:López-Parra, Virginia
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Mallavia, Beñat
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López-Franco, Óscar
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Ortiz-Muñoz, Guadalupe
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Oguiza, Ainhoa
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Recio, Carlota
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Blanco, Julia A Parra
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Nimmerjahn, F.
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Egido de los Ríos, Jesús
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Gómez-Guerrero, Carmen
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