51. Suppression of experimental glomerulonephritis by antiserum against transforming growth factor beta1
- Author
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Border, Wayne A., Okuda, Seiya, Languino, Lucia R., Sporn, Michael B., and Ruoslahti, Erkki
- Subjects
Glomerulonephritis -- Causes of ,Glomerulonephritis -- Models ,Transforming growth factors -- Physiological aspects ,Environmental issues ,Science and technology ,Zoology and wildlife conservation - Abstract
Glomerulonephritis is a disease characterized by the inflammation of the kidneys. The condition also causes an increase of protein and blood in the urine, a decrease in urine production, and a swelling of the body. The disease can progress, destroying kidney function completely, and can lead to the death of the patient unless treatment with dialysis or kidney transplantation is provided. The mechanism of disease in glomerulonephritis is not understood, but is thought to be due to cell injury in the glomeruli of the kidneys by the accumulation of immune complexes. Using experimentally induced glomerulonephritis in rats as an animal model, glomerulonephritis was shown to be associated with the increased synthesis and activity of the cellular factor transforming growth factor beta1 (TGF-beta1). TGF-beta1 is known to induce the production of extracellular matrix, an array of a fibrous connective tissue. Extracellular matrix accumulate in the damaged glomeruli in glomerulonephritis. When antibodies specific for TGF-beta1 were administered to the animals when the glomerular disease was experimentally induced, the amounts of extracellular matrix produced were reduced, and the disease did not develop. Thus, TGF-beta1 causes experimentally-induced glomerulonephritis, and may have a role in other fibrotic diseases. The inhibition of the action of TGF-beta may be a new approach for treatment of glomerulonephritis. (Consumer Summary produced by Reliance Medical Information, Inc.)
- Published
- 1990