Role of Intercellular Adhesion Molecule-1, Lymphocyte Function-associated Antigen-1, and Macrophages in ddY Mouse Nephropathy

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Title ( eng )
Role of Intercellular Adhesion Molecule-1, Lymphocyte Function-associated Antigen-1, and Macrophages in ddY Mouse Nephropathy
Creator
Ye Xue-Feng
Yorioka Noriaki
Oda Hiroaki
Taniguchi Yoshihiko
Yamakido Michio
Source Title
Hiroshima Journal of Medical Sciences
Volume 46
Issue 2
Start Page 75
End Page 80
Journal Identifire
[PISSN] 0018-2052
[EISSN] 2433-7668
[NCID] AA00664312
Abstract
ddY mouse nephropathy is an animal model of human IgA nephropathy that is characterized by spontaneous IgA deposition in the glomerular mesangium, mesangial cell proliferation, and matrix expansion. We investigated the involvement of intercellular adhesion molecule-1, lymphocyte function-associated antigen-1, and macrophages in the pathogenesis of ddY mouse nephropathy. Five mice each underwent urinalysis, light microscopic examination of the kidneys, immunofluorescent detection of immunoglobulins and complement, and immunohistochemical examination for intercellular adhesion molecule-1, lymphocyte function-associated antigen-1, and infiltrating macrophages at 5, 10, 20, 30, 40, 50, 60, and 70 weeks of age. Albuminuria was observed from the age of 20 weeks and all mice showed albuminuria by 70 weeks. Histological glomerular damage was significantly related to the appearance of albuminuria (p<0.01). In the glomeruli, positivity for intercellular adhesion molecule-1 and lymphocyte function-associated antigen-1, as well as the number of infiltrating macrophages, were significantly increased in mice with nephropathy compared to pre-nephropathy mice (p<0.01). These results suggest that intercellular adhesion molecule-1, lymphocyte function-associated antigen-1, and infiltrating macrophages are involved in the progression of histological damage in ddY mouse nephropathy.
Keywords
ddY mouse
Intercellular adhesion molecule-1
Lymphocyte function-associated antigen-1
Macrophages
NDC
Medical sciences [ 490 ]
Language
eng
Resource Type departmental bulletin paper
Publisher
Hiroshima University Medical Press
Date of Issued 1997-06
Publish Type Version of Record
Access Rights open access
Source Identifier
[ISSN] 0018-2052
[NCID] AA00664312