Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
SHR Neuro Krebs Kardio Lipid Stoffw Microb
Hochegger, K; Knight, S; Hugo, C; Mayer, G; Lawler, J; Mayadas, TN; Rosenkranz, AR.
Role of thrombospondin-1 in the autologous phase of an accelerated model of anti-glomerular basement membrane glomerulonephritis.
Nephron Exp Nephrol. 2004; 96(2):e31-e38
Doi: 10.1159/000076402
Web of Science
PubMed
FullText
FullText_MUG
- Führende Autor*innen der Med Uni Graz
- Eller Kathrin
- Rosenkranz Alexander
- Altmetrics:
- Dimensions Citations:
- Plum Analytics:
- Scite (citation analytics):
- Abstract:
- Background: Thrombospondin-1 (TSP1), a multifunctional, extracellular matrix protein, regulates cellular attachment, proliferation, migration, and differentiation in vitro, and is expressed de novo in many inflammatory diseases, including glomerulonephritis (GN). Methods: We investigated the role of TSP1 in the autologous phase of an accelerated model of anti-glomerular basement membrane (GBM) GN in mice deficient in TSP1. The model, induced by the injection of rabbit anti-mouse GBM antibody, is characterized by the development of proteinuria and glomerular damage over a 21-day observation period in wild-type mice. Results: Mice deficient in TSP1 developed significantly less proteinuria than their wild-type controls 21 days after induction of disease (5,793 +/- 5,456 vs. 24,293 +/- 15,336 mug albumin/mg creatinine; p = 0.002). Serum creatinine levels were significantly higher in the wild-type mice than in the TSP1 deficient animals (29.03 +/- 2.34 vs. 16.39 +/- 2.87 mumol/ l; p = 0.005). Other disease indices as crescent formation, fibrin deposition and macrophage influx, were also diminished in the TSP1 knockout animals. The numbers of interstitial CD4+ and CD8+ T cells were generally less in TSP1-deficient mice and reached statistical significance in CD4+ ( p = 0.01) and CD8+ T cells ( p = 0.02). The difference in outcome of the disease was not due to the difference in deposition/production of heterologous and autologous antibodies in the two groups of animals. Conclusion: This study suggests a proinflammatory role of TSP1 in an experimental model of GN. Copyright (C) 2004 S. Karger AG, Basel.
- Find related publications in this database (using NLM MeSH Indexing)
- Animals -
- Anti-Glomerular Basement Membrane Disease - immunology Anti-Glomerular Basement Membrane Disease - pathology
- Antibodies, Heterophile - analysis
- Isoantibodies - analysis
- Kinetics -
- Male -
- Mice -
- Mice, Knockout -
- Proteinuria - etiology
- Thrombospondin 1 - genetics Thrombospondin 1 - physiology
- Find related publications in this database (Keywords)
- thrombospondin-1
- transgenic mice
- glomerulonephritis