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Augmentation of osteopontin expression in renal tubuli is independent of a histopathological type of glomerular lesions in mouse lupus nephritis
Author(s) -
Sasaki Yoshifumi,
Yamamoto Yukisei,
Miyazaki Tatsuhiko,
Ito Mitsuko R.,
Nose Masato,
Watanabe Makoto
Publication year - 2006
Publication title -
pathology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
eISSN - 1440-1827
pISSN - 1320-5463
DOI - 10.1111/j.1440-1827.2006.01937.x
Subject(s) - lupus nephritis , osteopontin , pathology , kidney , in situ hybridization , systemic lupus erythematosus , nephritis , lesion , immunohistochemistry , renal cortex , medicine , biology , immunology , gene expression , gene , biochemistry , disease
Augmentation of osteopontin (OPN) expression in renal tubuli is often observed in lupus nephritis. To investigate whether this might depend on histopathological type of glomerular lesions, comparative studies of the distribution and levels of OPN expression in kidneys were performed by in situ hybridization and real‐time polymerase chain reaction in mouse lupus nephritis manifesting inflammatory (endocapillary proliferative) and deposit (wire loop) types of glomerular lesions. These glomerular lesions were developed in C.B‐17/Inc ‐scid/scid mice by injection of IgG3 antibody producing hybridoma clones, 2B11.3 and 7B6.8, respectively, which are derived from an MRL/Mp‐ lpr/lpr (MRL/lpr) lupus mouse. Both clones significantly augmented OPN expression in renal tubuli, but a non‐nephritogenic IgG3 clone, 1G3, derived from the same MRL/lpr mouse, did not. The OPN augmentation was prominent in the renal cortex and the inner stripe of the outer medulla. These results indicate that OPN augmentation in renal tubuli is not associated with a histopathological type of glomerular lesion in lupus nephritis, at least not with an inflammatory or a deposit type.

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