Publication: Class II lupus nephritis with podocyte injury in imiquimod-induced lupus-prone mice
Authors
Murai, Atsuko ; Yamazaki, Masaki ; Kito, Aki ; Nishihara, Kaori ; Oyama, Sohei ; Horiba, Naoshi ; Kato, Atsuhiko
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Publisher
Universidad de Murcia, Departamento de Biologia Celular e Histiologia
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DOI
https://doi.org/ 10.14670/HH-18-450
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info:eu-repo/semantics/article
Description
Abstract
Lupus nephritis (LN) is a renal disease
presented in systemic lupus erythematosus (SLE) and is
divided into 6 classes based on histopathological criteria
set by the International Society of Nephrology/Renal
Pathology Society. Major mouse models of SLE usually
develop class III/IV LN, which are characterized by
subendothelial deposits and endocapillary
hypercellularity. We examined the pathological features
of kidneys in a mouse model of SLE induced by a tolllike receptor 7 agonist, imiquimod (IMQ). In experiment
1, eleven-female FVB/NJcl wild type mice were treated
with IMQ on their ear skin 3 times per week. Plasma
anti-dsDNA increased from 2 weeks after first IMQ
treatment and 2 mice exhibited nephrotic syndrome from
6 weeks. Histopathology revealed eosinophilic
mesangial deposits in all mice from 4 weeks.
Subsequently, podocytes showed enlargement with
vacuolation and their numbers decreased in 6 mice.
There was no infiltration of inflammatory cells,
subendothelial deposits in glomeruli, or subepithelial
deposits in glomeruli. In experiment 2 using 10 mice at 8
weeks after IMQ treatment, the mesangial deposits were
observed in all mice and confirmed to be IgG, IgA, IgM,
C1q and C3 by immunofluorescence, which corresponds
to class II LN. Foot process effacement was detected by
transmission electron microscopy and was considered to
lead to proteinuria. These mice exhibited pathological
characteristics corresponding to class II LN and
podocyte injury, which make it distinct from other
mouse models of SLE
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Citation
Histology and Histopathology Vol. 37, nº7 (2022)
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