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Interaction of the small interstitial proteoglycans biglycan, decorin and fibromodulin with transforming growth factor beta.
- A. Hildebrand, M. Romarı́s, E. Ruoslahti
- Biology, Computer ScienceThe Biochemical journal
- 1 September 1994
The results show that the three decorin-type proteoglycans each bind TGF-beta isoforms and that slight differences exist in their binding properties, suggesting that the glycosaminoglycan chains may hinder the interaction of the core proteins with T GF-beta.
Transforming growth factor beta in tissue fibrosis.
Angiotensin II stimulates extracellular matrix protein synthesis through induction of transforming growth factor-beta expression in rat glomerular mesangial cells.
- S. Kagami, W. Border, D. Miller, N. Noble
- Biology, MedicineThe Journal of clinical investigation
- 1 June 1994
Results indicate that Ang II induces mesangial cell synthesis of matrix proteins and show that these effects are mediated by Ang II induction of TGF-beta expression, which may well contribute to glomerulosclerosis in vivo.
Transforming Growth Factor β in Tissue Fibrosis
A large number of patients with progressive fibrosis have no known underlying cause of disease and the prognosis is poor, suggesting that the disease is likely to get worse as they age.
Transforming growth factor-beta in disease: the dark side of tissue repair.
Natural inhibitor of transforming growth factor-β protects against scarring in experimental kidney disease
It is reported here that administration of decorin inhibits the increased production of extracellular matrix and attenuates manifestations of disease, confirming the hypothesis that decorin may eventually prove to be clinically useful in diseases associated with overproduction of TGF-β.
Renin increases mesangial cell transforming growth factor-beta1 and matrix proteins through receptor-mediated, angiotensin II-independent mechanisms.
It is concluded that renin upregulates MC TGF-beta1 through a receptor-mediated mechanism, independent of Ang II generation or action, and may contribute to renal fibrotic disease, particularly when therapeutic Ang II blockade elevates plasma renin.
Interactions of transforming growth factor-beta and angiotensin II in renal fibrosis.
The protective effect of inhibition of the renin-angiotensin system in experimental and human kidney diseases correlates closely with the suppression of transforming growth factor-beta production, suggesting that transforming growthfactor-beta, in addition to blood pressure, should be a therapeutic target.
Expression of transforming growth factor beta is elevated in human and experimental diabetic nephropathy.
- T. Yamamoto, T. Nakamura, N. Noble, E. Ruoslahti, W. Border
- Biology, MedicineProceedings of the National Academy of Sciences…
- 1 March 1993
It is reported that in glomeruli of rats made diabetic there is a slow, progressive increase in the expression of transforming growth factor beta (TGF- beta) mRNA and TGF-beta protein, which implicate TGF -beta in the pathogenesis of diabetic nephropathy.
Sustained expression of TGF-beta 1 underlies development of progressive kidney fibrosis.
We found that TGF-beta 1 expression and increased matrix production is transient and self-limited in nephritic glomeruli from rats with acute, reversible glomerulonephritis induced by a single…