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      Apoptotic Cell Loss following Cell Proliferation in Renal Glomeruli of Otsuka Long-Evans Tokushima Fatty Rats, a Model of Human Type 2 Diabetes

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          Abstract

          Background: The mechanism of glomerular cell loss during the late stage of diabetic nephropathy is unknown. Methods: We examined cell population, proliferation, apoptosis, and immunohistochemical expression of apoptosis-related proteins, Bcl-2 and Bax, in renal glomeruli of the Otsuka Long-Evans Tokushima Fatty (OLETF) rat, an animal model of human type 2 diabetes. 10-, 30-, 50-, and 70-week-old rats were used (n = 5–8). Control was the Long-Evans Tokushima Otsuka (LETO) rat. Results: The cell population in renal glomeruli of OLETF rats progressively increased with age, but decreased at 70 weeks old. High cell proliferative activity based on proliferating cell nuclear antigen (PCNA) expression was limited during the early stage, whereas by in situ nick end-labeling (TUNEL), Taq polymerase based in situ ligation, and electron microscopy, apoptosis was detected during the late stage (50 and 70 weeks old). Augmented expression of Bax, but not of Bcl-2, was evident in glomeruli of OLETF rats during the late stage, which contributed to an increased Bax/Bcl-2 ratio. Conclusion: It appears that high cell proliferative activity and the subsequent cell loss via apoptosis counterbalance each other and determine glomerular cell population of OLETF rats. Augmented Bax expression may be one of the important regulators of this apoptosis.

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          Most cited references 4

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          Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programed cell death

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            Structure-Function Analysis of Bcl-2 Protein

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              Glucose loading induces DNA fragmentation in rat proximal tubular cells.

               K Numakami,  H Itoh,  T Saruta (1996)
              A 10% glucose, 10% mannitol, or 0.9% saline solution was infused in male Wistar rats for 300 minutes via the left cervical vein. Glomerular filtration rates (GFRs) were not significantly altered in any of the three groups. DNA was extracted from isolated proximal tubular cells at the end of each infusion. Electrophoresis on agarose gels showed a distinct ladder pattern of DNA fragmentation in 10% glucose-loaded rats, but no such pattern in 10% mannitol- or 0.9% saline-loaded rats. After infusion for 300 minutes, the plasma glucose level of the 10% glucose-loaded group was higher than that of the other two groups (each P < .005). These results suggest that hyperglycemia led to DNA fragmentation in the DNA of proximal tubular cells, similar to the process of programmed cell death known as apoptosis. DNA fragmentation may be associated with renal proximal tubular damage in the early stages of diabetic nephropathy.
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                Author and article information

                Journal
                AJN
                Am J Nephrol
                10.1159/issn.0250-8095
                American Journal of Nephrology
                S. Karger AG
                0250-8095
                1421-9670
                2002
                December 2002
                07 October 2002
                : 22
                : 5-6
                : 587-595
                Affiliations
                aSecond Department of Internal Medicine, Gifu University School of Medicine, Gifu, and bDepartment of Food Science, Kyoto Women’s University, Kyoto, Japan
                Article
                65284 Am J Nephrol 2002;22:587–595
                10.1159/000065284
                12381965
                © 2002 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: 6, Tables: 1, References: 26, Pages: 9
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/65284
                Categories
                Laboratory Investigation

                Cardiovascular Medicine, Nephrology

                Apoptosis, Diabetes mellitus, Diabetic nephropathy, Glomerulus

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