RGD Reference Report - Effects of anti-TGF-beta type II receptor antibody on experimental glomerulonephritis. - Rat Genome Database

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Effects of anti-TGF-beta type II receptor antibody on experimental glomerulonephritis.

Authors: Kasuga, H  Ito, Y  Sakamoto, S  Kawachi, H  Shimizu, F  Yuzawa, Y  Matsuo, S 
Citation: Kasuga H, etal., Kidney Int. 2001 Nov;60(5):1745-55.
RGD ID: 1601601
Pubmed: PMID:11703592   (View Abstract at PubMed)
DOI: DOI:10.1046/j.1523-1755.2001.00990.x   (Journal Full-text)

BACKGROUND: Renal fibrosis, characterized by the accumulation of extracellular matrix (ECM), is a common histopathological feature of progressive renal disease of diverse etiology. Interaction between transforming growth factor-beta (TGF-beta) and TGF-beta type II receptor (TGF-betaIIR) may play an important role in the ongoing fibrotic process. TGF-betaIIR and TGF-beta have been reported to be up-regulated in human glomerulopathies. In order to block the TGF-beta system, many studies have inhibited TGF-beta itself, but not its receptors. Our study explored the effects of fully human monoclonal antibody against TGF-betaIIR (hTGF-betaIIRAb) on experimental proliferative glomerulonephritis. METHODS: hTGF-betaIIRAb was generated from Xenomice. The expression of TGF-betaIIR was studied by immunohistochemistry in normal and anti-Thy-1 nephritis rats. hTGF-betaIIRAb or control Ab was injected intraperitoneally at day 0 and day 4 of anti-Thy-1 nephritis, and rats were sacrificed at day 7. Effects of hTGF-betaIIRAb were assessed by histological and immunopathological measurements. RESULTS: The specificity of hTGF-betaIIRAb was confirmed by ELISA and Western blot analysis. By immunostaining, TGF-betaIIR expression was up-regulated in the proliferative lesions of anti-Thy-1 nephritis at day 7. In the hTGF-betaIIRAb-treated group, the extent of mesangial expansion was less than that in the control group. By immunohistology, alpha-smooth muscle actin, fibronectin-EDA, and type I collagen were significantly reduced in the hTGF-betaIIRAb-treated group. CONCLUSIONS: Anti-TGF-betaIIR antibody ameliorated ECM accumulation in anti-Thy-1 nephritis. Our data suggest that TGF-betaIIR may be one of the therapeutic targets, and that fully human monoclonal antibody against TGF-betaIIR may have a new therapeutic potential for renal fibrosis.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
membranoproliferative glomerulonephritis  ISOTgfbr2 (Rattus norvegicus)1601601; 1601601 RGD 
membranoproliferative glomerulonephritis  IDA 1601601 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Tgfbr2  (transforming growth factor, beta receptor 2)

Genes (Mus musculus)
Tgfbr2  (transforming growth factor, beta receptor II)

Genes (Homo sapiens)
TGFBR2  (transforming growth factor beta receptor 2)


Additional Information