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      Urinary Transforming Growth Factor-β (TGF-β) Excretion and Renal Production of TGF-β in Rats with Subtotal Renal Ablation: Effect of Enalapril and Nifedipine

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          The aim of the present study was to investigate the effect of enalapril and nifedipine on renal transforming growth factor-β (TGF-β) production and on the rate of urinary TGF-β excretion in rats with subtotal renal ablation. After subtotal nephrectomy some animals were treated with enalapril or nifedipine. Renal cortical TGF-β mRNA levels were 68% higher in untreated nephrectomized rats (p < 0.05) and 39% higher in rats treated with nifedipine (p < 0.05) compared with controls. There was no difference in renal cortical TGF-β mRNA content between the nephrectomized rats treated with enalapril and sham animals, showing that enalapril treatment prevented the increase of TGF-β mRNA in nephrectomized rats. The rate of urinary TGF-β excretion was 2.2 ± 0.8 pg/min in sham animals, 61.5 ± 40.1 pg/min in untreated nephrectomized rats, 9.6 ± 4.2 pg/min in nephrectomized rats treated with enalapril, and 55.2 ± 24.46 pg/min in rats treated with nifedipine. The immunohistochemical reaction for TGF-β in the renal cortex was less intense in the nephrectomized rats treated with enalapril than in the other groups of rats with subtotal renal ablation. These data show that enalapril induces a decrease in renal TGF-β production and in urinary TGF-β excretion in rats with subtotal renal ablation, an effect associated with the protective action of this treatment on renal structure and function and suggest that the determination of the rate of urinary TGF-β could be a useful procedure for the evaluation of disease progression and therapeutic efficacy in the remnant kidney model.

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          Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction.

          A new method of total RNA isolation by a single extraction with an acid guanidinium thiocyanate-phenol-chloroform mixture is described. The method provides a pure preparation of undegraded RNA in high yield and can be completed within 4 h. It is particularly useful for processing large numbers of samples and for isolation of RNA from minute quantities of cells or tissue samples.
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            Natural inhibitor of transforming growth factor-beta protects against scarring in experimental kidney disease.

            The central pathological feature of human kidney disease that leads to kidney failure is the accumulation of extracellular matrix in glomeruli. Overexpression of transforming growth factor-beta (TGF-beta) underlies the accumulation of pathological matrix in experimental glomerulonephritis. Administration of an antibody raised against TGF-beta to glomerulonephritic rats suppresses glomerular matrix production and prevents matrix accumulation in the injured glomeruli. One of the matrix components induced by TGF-beta, the proteoglycan decorin, can bind TGF-beta and neutralize its biological activity, so decorin may be a natural regulator of TGF-beta (refs 3, 4). We tested whether decorin could antagonize the action of TGF-beta in vivo using the experimental glomerulonephritis model. We report here that administration of decorin inhibits the increased production of extracellular matrix and attenuates manifestations of disease, confirming our hypothesis. On the basis of our results, decorin may eventually prove to be clinically useful in diseases associated with overproduction of TGF-beta.
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              Suppression of experimental glomerulonephritis by antiserum against transforming growth factor beta 1.

              Glomerulonephritis is an inflammation of the kidney characterized by the accumulation of extracellular matrix within the damaged glomeruli, impaired filtration and proteinuria. In its progressive form, the disease destroys kidney function leading to uraemia and death, unless dialysis therapy or kidney transplantation is available. The pathogenesis of glomerulonephritis is incompletely understood, but the eliciting factor is thought often to be an immunological injury to mesangial and/or other resident cells in the glomeruli. We have used an animal model of acute mesangial proliferative glomerulonephritis to show that this disease is associated with increased production and activity of transforming growth factor beta 1 (TGF-beta 1), an inducer of extracellular matrix production. Here we report that administration of anti-TGF-beta 1 at the time of induction of the glomerular disease suppresses the increased production of extracellular matrix and dramatically attenuates histological manifestations of the disease. These results provide direct evidence for a causal role of TGF-beta 1 in the pathogenesis of the experimental disease and suggest a new approach to the therapy of glomerulonephritis.

                Author and article information

                S. Karger AG
                March 1998
                25 February 1998
                : 78
                : 3
                : 302-309
                Departments of a Physiology, b Pathology and c Internal Medicine, Medical School of Ribeirão Prêto, University of São Paulo, Ribeirão Prêto, SP, Brazil
                44940 Nephron 1998;78:302–309
                © 1998 S. Karger AG, Basel

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                Page count
                Figures: 5, Tables: 1, References: 42, Pages: 8
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/44940
                Original Paper


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