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Blockade of CCL2/CCR2 signalling ameliorates diabetic nephropathy in db/db mice

Authors
Seok, Su JinLee, Eun SooKim, Geun TaeHyun, MiriLee, Ji-HyeChen, SheldonChoi, RanKim, Hong MinLee, Eun YoungChung, Choon Hee
Issue Date
Jul-2013
Publisher
Oxford University Press
Keywords
albuminuria; CCL2; CCR2; diabetic nephropathy
Citation
Nephrology Dialysis Transplantation, v.28, no.7, pp 1700 - 1710
Pages
11
Journal Title
Nephrology Dialysis Transplantation
Volume
28
Number
7
Start Page
1700
End Page
1710
URI
https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/13564
DOI
10.1093/ndt/gfs555
ISSN
0931-0509
1460-2385
Abstract
Background. CCL2/C-C chemokine receptor 2 (CCR2) signalling is suggested to play a significant role in various kidney diseases including diabetic nephropathy. We investigated the renoprotective effect of a CCR2 antagonist, RS102895, on the development of diabetic nephropathy in a type 2 diabetic mouse model. Methods. Six-week-old diabetic db/db and non-diabetic db/m mice were fed either normal chow or chow mixed with 2 mg/kg/day of RS102895 for 9 weeks. We investigated the effects of CCR2 antagonism on blood glucose, blood pressure, albuminuria and the structure and ultrastructure of the kidney. Results. Diabetes-induced albuminuria was significantly improved after CCR2 antagonist treatment, and glucose intolerance was improved in the RS102895-treated diabetic mice. RS102895 did not affect blood pressure, body weight or kidney weight. Mesangial expansion, glomerular basement membrane thickening and increased desmin staining in the diabetic kidney were significantly improved after RS102895 treatment. The up-regulation of vascular endothelial growth factor mRNA expression and the down-regulation of nephrin mRNA expression were markedly improved in the kidneys of RS102895-treated diabetic mice. Increased renal CD68 and arginase II and urinary malondialdehyde in diabetes were effectively attenuated by RS102895 treatment. Conclusion. Blockade of CCL2/CCR2 signalling by RS102895 ameliorates diabetic nephropathy not only by improving blood glucose levels but also by preventing CCL2/CCR2 signalling from altering renal nephrin and VEGF expressions through blocking macrophage infiltration, inflammation and oxidative stress in type 2 diabetic mice.
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