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Daniel, C. et al.

Thrombospondin-1 is a major activator of TGF-beta in fibrotic renal disease in the rat in vivo.

BACKGROUND: Transforming growth factor-beta ( TGF-beta), a profibrotic cytokine involved in many scarring processes, has to be activated extracellularly before it can bind to its receptors. Thrombospondin 1 (TSP1), a multifunctional matricellular glycoprotein, has been identified as an activator of TGF-beta in in vitro systems and during mouse postnatal development in vivo. TSP1 is expressed de novo in many inflammatory disease processes, including glomerular disease. METHODS: In this study we investigated whether peptides specifically interfering with the activation process of TGF-beta by TSP1 may be able to block activation of TGF-beta in an in vivo model of mesangial proliferative glomerulonephritis. RESULTS: Continuous intravenous infusion of blocking peptide by minipumps significantly reduced expression of active TGF-beta in glomeruli on day 7 of disease as indicated by immunohistochemistry, bioassay, and activation of the TGF-beta signal transduction pathway, while total TGF-beta expression was unchanged. Inhibition of glomerular TGF-beta activation was accompanied by a decrease of glomerular extracellular matrix accumulation and proteinuria, but was without effect on mesangial cell proliferation or influx of monocytes/macrophages. CONCLUSION: TSP1 is a major endogenous activator of TGF-beta in experimental inflammatory glomerular disease. Drugs interfering with the activation of TGF-beta by locally produced TSP1 may be considered as a future specific treatment of scarring kidney disease.[1]

References

Thrombospondin-1 is a major activator of TGF-beta in fibrotic renal disease in the rat in vivo. Daniel, C., Wiede, J., Krutzsch, H.C., Ribeiro, S.M., Roberts, D.D., Murphy-Ullrich, J.E., Hugo, C. Kidney Int. (2004) [Pubmed]

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