Expression of Transforming Growth Factor-beta and Morphologic Changes of Glomerulosclerosis in FGS/NgaKist Mouse.
- Author:
Hoon Kyu OH
;
Yong Jin KIM
;
Mi Ok PARK
;
Chul Ho LEE
;
Byung Hwa HYUN
;
In Soo SHU
- Publication Type:Original Article
- Keywords:
FGS/NgaKist mouse;
FSGS;
TGF-beta;
In-situ hybridization
- MeSH:
Aging;
Animals;
Collagen;
Complement System Proteins;
Endothelial Cells;
Extracellular Matrix;
Glomerulosclerosis, Focal Segmental;
Immunoglobulin A;
Immunoglobulin G;
Immunoglobulin M;
Mice*;
Models, Animal;
Proteinuria;
Renal Insufficiency;
RNA, Messenger;
Sclerosis;
Transforming Growth Factor beta
- From:Korean Journal of Pathology
1998;32(1):35-42
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Focal segmental glomerulosclerosis (FSGS) is presented as not only one of the primary glomerular diseases but also as a secondary phenomenon for chronic irreversible renal diseases. The main pathological feature of FSGS is the accumulation of extracellular matrix in the glomeruli, for which overexpression of transforming growth factor-beta (TGF-beta) may be responsible for the accumulation of pathological matrix. A new animal model (FGS/NgaKist mouse) of renal failure by spontaneously generating glomerulosclerosis was developed. To elucidate the role of TGF-beta for FSGS, authors observed glomeruli of FGS/NgaKist mouse periodically. FGS/NgaKist mouse strain showed progression of proteinuria and focal glomerular sclerosis with the aging. The glomeruli showed anti IgG, IgA, IgM and complement complex deposits and extracellular matrix accumulation in the mesangium. TGF-beta mRNA and beta2antibody expressions were increased with the advance of glomerular sclerosis. The results suggest the following; FSGS of FGS/NgaKist strain is immune mediated disease and this stimuli on mesangial or endothelial cells may activate TGF-beta gene in their nuclei. This activation, in turn, can cause sclerosis by increasing TGF-beta mRNA transcription followed by secretion of TGF-beta and its action as cytokine for making collagen fibrils.
