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Research Article Free access | 10.1172/JCI118697
Division of Nephrology, Department of Medicine, University of Washington, Seattle, Washington 98195, USA.
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Division of Nephrology, Department of Medicine, University of Washington, Seattle, Washington 98195, USA.
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Division of Nephrology, Department of Medicine, University of Washington, Seattle, Washington 98195, USA.
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Division of Nephrology, Department of Medicine, University of Washington, Seattle, Washington 98195, USA.
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Division of Nephrology, Department of Medicine, University of Washington, Seattle, Washington 98195, USA.
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Division of Nephrology, Department of Medicine, University of Washington, Seattle, Washington 98195, USA.
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Division of Nephrology, Department of Medicine, University of Washington, Seattle, Washington 98195, USA.
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Division of Nephrology, Department of Medicine, University of Washington, Seattle, Washington 98195, USA.
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Division of Nephrology, Department of Medicine, University of Washington, Seattle, Washington 98195, USA.
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Published June 1, 1996 - More info
The expression of the two cytoskeletal linking proteins, moesin and radixin, was examined in experimental mesangial proliferative nephritis in rats (anti-Thy1 model). Moesin and radixin mRNA and protein are constitutively expressed in all cell types of normal rat glomeruli, except podocytes. In the anti-Thy1 model the expression of moesin and radixin was increased in infiltrating macrophages and in activated, alpha-smooth muscle actin-positive mesangial cells and was concentrated in the cellular extensions of mesangial cells in areas of glomerular remodelling. Studies using neutralizing antibodies demonstrated that the increase in moesin and radixin expression by mesangial cells is mediated by PDGF, but not bFGF. The increase in these cytoskeletal proteins appears to be regulated primarily (radixin) or partially (moesin) posttranscriptionally. The data suggest that PDGF mediated upregulation of the cytoskeletal proteins, moesin and radixin, is important for cell migration and other changes that accompany the coordinated restoration of glomerular architecture after injury.