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      Ultrastructural Localization of Dominantly Increased Fibronectin in the Markedly Thickened Glomerular Basement Membrane in a Selectively Mated Murine High IgA Strain (HIGA Mice)

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          Abstract

          To clarify which matrix component(s) contributes to glomerular sclerosis with mesangial IgA deposits in a murine high serum IgA strain (HIGA) derived from ddY mice, morphological and immunopathological analyses of glomeruli were performed in comparison with original ddY and BALB/c mice as controls. Significantly increased thickness of the glomerular basement membrane (GBM), especially the lamina densa, was observed in HIGA mice. Immunofluorescent staining showed marked increases in levels of fibronectin and laminin in both the mesangium and capillary wall in aged HIGA mice. Analysis of the distribution of immunogold-labeled antibody in GBM revealed a significant increase (p < 0.0001) and specific orientation of fibronectin in the endothelial side, which suggested that mesangial fibronectin produced at high levels due to IgA deposition extended to the endothelial side of GBM and contributed to the thickening of GBM with further development to glomerulosclerosis in the HIGA mice.

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          Most cited references4

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          The renal glomerulus of mice lacking s-laminin/laminin beta 2: nephrosis despite molecular compensation by laminin beta 1.

          S-laminin/laminin beta 2, a homologue of the widely distributed laminin B1/beta 1 chain, is a major component of adult renal glomerular basement membrane (GBM). Immature GBM bears beta 1, which is replaced by beta 2 as development proceeds. In mutant mice that lack beta 2, the GBM remains rich in beta 1, suggesting that a feedback mechanism normally regulates GBM maturation. The beta 2-deficient GBM is structurally intact and contains normal complements of several collagenous and noncollagenous glycoproteins. However, mutant mice develop massive proteinuria due to failure of the glomerular filtration barrier. These results support the idea that laminin beta chains are functionally distinct although they assemble to form similar structures. Laminin beta 2-deficient mice may provide a model for human congenital or idiopathic nephrotic syndromes.
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            Fibronectins: multifunctional modular glycoproteins

            R O Hynes (1982)
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              Quantitative changes in the glomerular basement membrane components in human membranous nephropathy.

              S Lee, J. Zhang (1997)
              In membranous nephropathy (MN), the glomerular basement membrane (GBM) is thickened due to accumulation of GBM material between and around the subepithelial immune deposits. Alterations in the GBM components in relation to subepithelial deposits and GBM thickening are not clearly defined. The GBM distribution of classical and novel [alpha 4(IV)] chains of type IV collagen, laminin, and fibronectin have been studied in seven patients with MN and in three normal controls by a quantitative immunogold technique. In normal kidneys, the labelling of type IV collagen or fibronectin was distributed predominantly along the endothelial side of the GBM; alpha 4(IV) was found in the lamina densa; and laminin was concentrated in the epithelial zone of the GBM (P < 0.01). In MN, there were increased immunogold densities for classical and novel type IV collagen chains, laminin, and fibronectin in the spikes of MN patients compared with controls (P < 0.05). Furthermore, gold particle labelling for the alpha 4(IV) collagen chain was increased in the middle zone (P < 0.01) and that for fibronectin was increased in the endothelial and middle zones of the GBM (P < 0.05) compared with normal controls. These findings suggest that subepithelial immune deposits stimulate glomerular epithelial cells (GEC), resulting in enhanced secretion of classical and novel type IV collagen chains, laminin, and fibronectin, forming spikes in MN; of these newly formed components, only novel type IV collagen appears to migrate towards the middle zone of the GBM, contributing to thickening of this zone. The results also suggest that fibronectin, possibly derived from the circulation, is related to thickening of the endothelial zone of the GBM, which in turn might be related to progressive glomerulosclerosis.
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                Author and article information

                Journal
                NEF
                Nephron
                10.1159/issn.1660-8151
                Nephron
                S. Karger AG
                1660-8151
                2235-3186
                1999
                October 1999
                22 September 1999
                : 83
                : 2
                : 146-153
                Affiliations
                aDepartment of Cardiovascular Medicine, Kyoto University, Graduate School of Medicine and bNippon Shinyaku, Kyoto, and cKitano Hospital, Osaka, Japan
                Article
                45492 Nephron 1999;83:146–153
                10.1159/000045492
                10516494
                c8f23317-8303-40ca-9dd4-ddd2e88d2c00
                © 1999 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                Page count
                Figures: 6, Tables: 2, References: 35, Pages: 8
                Categories
                Original Paper

                Cardiovascular Medicine,Nephrology
                ddY mouse,Fibronectin,HIGA mouse,Immunoelectron microscopy,IgA nephropathy

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