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      Crescent-Forming Mechanism in an Irreversible Thy-1 Model in Rats

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          Abstract

          Background: The crescent-forming mechanism has not yet been fully clarified and a cell which constitutes a crescent still remains controversial. This study was undertaken to analyze the crescent-forming mechanism in an irreversible Thy-1 model by applying a new marker-recognizing monoclonal antibody (mAb) OS-3. Methods: An irreversible Thy-1 model was induced by an intravenous injection of 500 µg of anti-Thy-1 mAb 1-22-3 to unilaterally nephrectomized Wistar rats. Seven rats were sacrificed 3, 7 and 14 days after the mAb injection respectively and the renal tissues were examined histologically and immunohistochemically. Results: Inflammatory cells were demonstrated mostly in the interstitium, but they were located within advanced cellular crescents in later stages. OS-3, which stained parietal glomerular epithelial cell (PGEC) only partly in a normal rat kidney section, reacted to PGEC more extensively at day 3 and also with cellular crescents at day 7. During the course of this model the podocytes lost their characteristic to be stained by anti-podocalyxcin Ab and obtained a new marker of a diseased state, i.e. to be positively stained by OS-3. Conclusion: Glomerular epithelial cells, but not inflammatory cells, are suggested to directly participate in the crescent formation in early stages, and podocytes with phenotypic changes might be partly involved in the formation of the crescents.

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          Most cited references 3

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          RANTES and Monocyte Chemoattractant Protein–1 (MCP-1) Play an Important Role in the Inflammatory Phase of Crescentic Nephritis, but Only MCP-1 Is Involved in Crescent Formation and Interstitial Fibrosis

          The involvement of chemokines in inflammation is well established, but their functional role in disease progression, and particularly in the development of fibrosis, is not yet understood. To investigate the functional role that the chemokines monocyte chemoattractant protein–1 (MCP-1) and RANTES play in inflammation and the progression to fibrosis during crescentic nephritis we have developed and characterized a murine model for this syndrome. Significant increases in T-lymphocytes and macrophages were observed within glomeruli and interstitium, paralleled by an induction of mRNA expression of MCP-1 and RANTES, early after disease initiation. Blocking the function of MCP-1 or RANTES resulted in significant decreases in proteinuria as well as in numbers of infiltrating leukocytes, indicating that both MCP-1 and RANTES (regulated upon activation in normal T cells expressed and secreted) play an important role in the inflammatory phase of crescentic nephritis. In addition, neutralization of MCP-1 resulted in a dramatic decrease in both glomerular crescent formation and deposition of type I collagen. These results highlight a novel role for MCP-1 in crescent formation and development of interstitial fibrosis, and indicate that in addition to recruiting inflammatory cells this chemokine is critically involved in irreversible tissue damage.
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            Renal catabolism of advanced glycation end products: the fate of pentosidine.

            Advanced glycation end products (AGEs) generated through the Maillard reaction significantly alter protein characteristics. Their accumulation has been incriminated in tissue injury associated with aging, diabetes, and renal failure. However, little is known about their clearance from the body. The present study delineates the catabolic pathway of a well-defined AGE product, pentosidine. Synthesized pentosidine given intravenously in rats with normal renal function was rapidly eliminated from the circulation through glomerular filtration, but was undetectable in the urine by chemical analysis. Immunohistochemistry with anti-pentosidine antibody disclosed that pentosidine accumulated transiently in the proximal renal tubule one hour after its administration, but had disappeared from the kidney at 24 hours. After an intravenous load of radiolabeled pentosidine, radioactivity peaked in the kidney at one hour and subsequently decreased, whereas it rose progressively in the urine. Over 80% of the radioactivity was recovered in the 72-hour collected urine. However, only 20% of urine radioactivity was associated with intact pentosidine chemically or immunochemically. In gentamicin-treated rats with tubular dysfunction, up to 30% of the pentosidine load was recovered as intact pentosidine in the urine. The present study suggests that free pentosidine (and possibly other AGEs) is filtered by renal glomeruli, reabsorbed in the proximal tubule where it is degraded or modified, and eventually excreted in the urine. Kidney thus plays a key role in pentosidine disposal.
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              Clinicopathological significance of intratubular giant macrophages in progressive glomerulonephritis

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                Author and article information

                Journal
                NEF
                Nephron
                10.1159/issn.1660-8151
                Nephron
                S. Karger AG
                1660-8151
                2235-3186
                2001
                2001
                22 November 2001
                : 89
                : 4
                : 439-447
                Affiliations
                Department of aCell Biology, Institute of Nephrology, bInternal Medicine II and cCollege of Biomedical Technology, Niigata University School of Medicine, Niigata, Japan
                Article
                46117 Nephron 2001;89:439–447
                10.1159/000046117
                11721163
                © 2001 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.

                Page count
                Figures: 7, Tables: 1, References: 22, Pages: 9
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/46117
                Categories
                Original Paper

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