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Endogenous fibroblast growth factor-2 mediates cytotoxicity in experimental mesangioproliferative glomerulonephritis.

J Floege, M Burg, C Hugo, K L Gordon, H Van Goor, M Reidy, W G Couser, K M Koch and R J Johnson
JASN May 1998, 9 (5) 792-801; DOI: https://doi.org/10.1681/ASN.V95792
J Floege
Division of Nephrology, Medizinische Hochschule, Hannover, Germany.
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M Burg
Division of Nephrology, Medizinische Hochschule, Hannover, Germany.
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C Hugo
Division of Nephrology, Medizinische Hochschule, Hannover, Germany.
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K L Gordon
Division of Nephrology, Medizinische Hochschule, Hannover, Germany.
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H Van Goor
Division of Nephrology, Medizinische Hochschule, Hannover, Germany.
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M Reidy
Division of Nephrology, Medizinische Hochschule, Hannover, Germany.
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W G Couser
Division of Nephrology, Medizinische Hochschule, Hannover, Germany.
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K M Koch
Division of Nephrology, Medizinische Hochschule, Hannover, Germany.
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R J Johnson
Division of Nephrology, Medizinische Hochschule, Hannover, Germany.
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Abstract

Fibroblast growth factor-2 (FGF-2) is released from mesangial cells in experimental mesangioproliferative glomerulonephritis induced with anti-Thy 1.1 antibody. To investigate the functional role of released FGF-2, rats received either neutralizing anti-FGF-2 IgG or a functional peptide antagonist of FGF-2 (FGF119-126) before or shortly after induction of anti-Thy 1.1 nephritis. In additional experiments, rats were treated with bolus injections of FGF-2 from 2 to 6 h after disease induction. The data showed that anti-FGF-2 therapy led to significant reductions of early mesangial cell injury (mesangiolysis, microaneurysm formation) and the subsequent mesangioproliferative changes (glomerular de novo expression of alpha-smooth muscle actin, mesangial cell proliferation, matrix accumulation, and platelet influx). Conversely, injections of FGF-2 augmented both mesangial injury and the subsequent mesangioproliferative changes. Studies on the mechanisms underlying the amplification of mesangial cell injury by FGF-2 showed that anti-FGF-2 therapy reduced cell death at 2 and 8 h after disease induction by 58 and 54%, respectively. This was associated with significant reductions in the number of glomerular H2O2- and OH -producing cells, as well as reduced glomerular production of nitric oxide. These data suggest that release of constitutively expressed FGF-2 after immune-mediated cell injury contributes to glomerular cell damage and thus identify FGF-2 as a novel mediator of cytotoxicity.

  • Copyright © 1998 by American Society of Nephrology
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Journal of the American Society of Nephrology
Vol. 9, Issue 5
1 May 1998
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Endogenous fibroblast growth factor-2 mediates cytotoxicity in experimental mesangioproliferative glomerulonephritis.
J Floege, M Burg, C Hugo, K L Gordon, H Van Goor, M Reidy, W G Couser, K M Koch, R J Johnson
JASN May 1998, 9 (5) 792-801; DOI: 10.1681/ASN.V95792

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Endogenous fibroblast growth factor-2 mediates cytotoxicity in experimental mesangioproliferative glomerulonephritis.
J Floege, M Burg, C Hugo, K L Gordon, H Van Goor, M Reidy, W G Couser, K M Koch, R J Johnson
JASN May 1998, 9 (5) 792-801; DOI: 10.1681/ASN.V95792
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