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      Oxidative Stress Decreases Klotho Expression in a Mouse Kidney Cell Line

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          Abstract

          Background/Aims: Defects in klotho gene expression in the mouse result in a syndrome that resembles human aging. We recently identified expression of klotho in a mouse inner medullary collecting duct (mIMCD3) cell line for the first time, and in the present study we explored the physiological relevance of the regulation of klotho expression in the presence of oxidant stress injury. Methods: Klotho expression was analyzed by real-time PCR, Western blot, and immuocytochemical staining during exposure to hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>). Overexpression of the klotho gene was induced by klotho adenoviruses, and the number of apoptotic cells was counted by flowcytometry. Results: Oxidant stress injury by H<sub>2</sub>O<sub>2 </sub>dose-dependently reduced klotho expression and diminished klotho staining. There were fewer apoptotic cells among the klotho-transfected cells than among the control cells. Conclusion: Klotho is expressed in cell line mIMCD3, and the klotho gene may be involved in the process of oxidative stress injury and apoptosis in this cell line.

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          Severely reduced production of klotho in human chronic renal failure kidney.

          N Koh, T Fujimori, S Nishiguchi … (2001)
          We recently identified a novel gene, termed klotho (kl) that is involved in the development of a syndrome in mice resembling human aging. A defect of the kl gene expression in mice leads to multiple disorders including arteriosclerosis, osteoporosis, ectopic calcification, and skin atrophy together with short life-span and infertility. Patients with chronic renal failure (CRF), develop multiple complications that are reminiscent of phenotypes observed in kl mutant mice. Furthermore, the kl gene is mainly expressed in kidney and brain. These evidences above suggest the possible involvement of Klotho function in the complications arising in CRF patients. To investigate the above possibility, we examined the kidneys of 10 clinically or histologically diagnosed CRF cases. The level of kl gene expression was measured by utilizing RNase protection assay. The expression of Klotho protein was assayed by utilizing Western blot analysis and by immunohistochemistry. The levels of kl mRNA expression were greatly reduced in all CRF kidneys. Moreover, the production of Klotho protein was also severely reduced in all CRF kidneys. These results suggest that the decrease in kl gene expression in CRF patients may underlie the deteriorating process of multiple complications in the CRF patients. Copyright 2001 Academic Press.
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            Structure of the mouse klotho gene and its two transcripts encoding membrane and secreted protein.

            A. Iida, S Sekine, Y Nabeshima … (1998)
            We previously established a novel mouse model for human aging and identified the genetic foundation responsible for it. A defect in expression of a novel gene, termed klotho (kl), leads to a syndrome resembling human aging in mice. The kl gene encodes a single-pass membrane protein whose extracellular domain carries homology to beta-glucosidases. In this report, we present the entire mouse kl gene organization. The mouse kl gene spans about 50 kilobases and consists of five exons. The promoter region lacks a TATA-box and contains four potential binding sites for SP1. We further show that two kl gene transcripts encoding membrane or secreted protein are generated through alternative transcriptional termination. These findings provide fundamental information for further study of the kl gene which may regulate aging in vivo.
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              Reactive oxygen species and acute renal failure.

              Karl A. Nath, Suzanne M. Norby (2000)
              Acute renal failure is commonly due to acute tubular necrosis (ATN), the latter representing an acute, usually reversible loss of renal function incurred from ischemic or nephrotoxic insults occurring singly or in combination. Such insults instigate a number of processes-hemodynamic alterations, aberrant vascular responses, sublethal and lethal cell damage, inflammatory responses, and nephron obstruction-that initiate and maintain ATN. Eventually, reparative and regenerative processes facilitate the resolution of renal injury and the recovery of renal function. Focusing mainly on ischemic ATN, this article reviews evidence indicating that the inordinate or aberrant generation of reactive oxygen species (ROS) may contribute to the initiation and maintenance of ATN. This review also discusses the possibility that ROS may instigate adaptive as well as maladaptive responses in the kidney with ATN, and raises the possibility that ROS may participate in the recovery phase of ATN.
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                Author and article information

                Journal
                Journal ID (publisher-id): NEE
                Journal ID (nlm-ta): Nephron Exp Nephrol
                Journal ID (doi): 10.1159/issn.1660-2129
                Title: Cardiorenal Medicine
                Publisher: S. Karger AG
                ISSN (Electronic): 1660-2129
                Publication date Subscription-year: 2005
                Publication date (Print): October 2005
                Publication date (Electronic): 22 June 2005
                Volume: 101
                Issue: 2
                Pages: e67-e74
                Affiliations
                Departments of aMedicine IV, and bBlood Purification, Tokyo Women’s Medical University, Tokyo, Japan
                Article
                Publisher ID: 86500 Other ID: Nephron Exp Nephrol 2005;101:e67–e74
                DOI: 10.1159/000086500
                PubMed ID: 15976510
                SO-VID: 1bf3b38f-5abd-45a9-8f57-62b943b76f7c
                Copyright © © 2005 S. Karger AG, Basel
                License:

                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
                Date received : 28 February 2005
                Date accepted : 04 April 2005
                Page count
                Figures: 6, References: 25, Pages: 1
                Categories
                Subject: Original Paper

                ScienceOpen disciplines: Cardiovascular Medicine,Nephrology
                Keywords: Hydrogen peroxide,Oxidative stress,Adenovirus,Flowcytometry,Klotho,Apoptosis,Real-time PCR,Collecting duct
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine, Nephrology
                Keywords: Hydrogen peroxide, Oxidative stress, Adenovirus, Flowcytometry, Klotho, Apoptosis, Real-time PCR, Collecting duct

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