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      Accelerated Recovery of Glycerol-Induced Acute Renal Failure in Rats with Previous Partial Hepatectomy

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          Abstract

          Several studies have reported a favorable effect following the administration of growth factors during the course of acute renal failure. To evaluate the effect of an increased endogenous production of growth factors, rats underwent 70% hepatectomy before glycerol-induced acute renal failure. The renal function was then monitored 12 and 48 h after glycerol injection in conscious rats. Twelve hours after the induction of acute renal failure, a reduction in creatinine clearance and sodium reabsorption was seen in both prehepatectomized and sham-hepatectomized rats. At 48 h, there was total recovery of glomerular filtration and tubular function in the prehepatectomized rats, whereas the sham-hepatectomized rats still had reduced glomerular filtration and sodium reabsorption. In rats treated with dexamethasone before hepatectomy and studied 48 h after the induction of acute renal failure, the protective action on renal function seen in prehepatectomized rats was totally blocked. A semiquantitative histological analysis done 48 h after the induction of acute renal failure demonstrated a fourfold increase in the number of necrotic tubules in both sham-hepatectomized and dexamethasone-treated rats as compared with hepatectomized rats. It is concluded that partial hepatectomy, a maneuver used to increase the endogenous synthesis of growth factors, accelerates recovery of renal function following glycerol-induced acute renal failure.

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          Most cited references 3

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          Scatter factor/hepatocyte growth factor and its receptor, the c-met tyrosine kinase, can mediate a signal exchange between mesenchyme and epithelia during mouse development

          Scatter factor/hepatocyte growth factor (SF/HGF) has potent motogenic, mitogenic, and morphogenetic activities on epithelial cells in vitro. The cell surface receptor for this factor was recently identified: it is the product of the c-met protooncogene, a receptor-type tyrosine kinase. We report here the novel and distinct expression patterns of SF/HGF and its receptor during mouse development, which was determined by a combination of in situ hybridization and RNase protection experiments. Predominantly, we detect transcripts of c-met in epithelial cells of various developing organs, whereas the ligand is expressed in distinct mesenchymal cells in close vicinity. In addition, transient SF/HGF and c-met expression is found at certain sites of muscle formation; transient expression of the c-met gene is also detected in developing motoneurons. SF/HGF and the c-met receptor might thus play multiple developmental roles, most notably, mediate a signal given by mesenchyme and received by epithelial. Mesenchymal signals are known to govern differentiation and morphogenesis of many epithelia, but the molecular nature of the signals has remained poorly understood. Therefore, the known biological activities of SF/HGF in vitro and the embryonal expression pattern reported here indicate that this mesenchymal factor can transmit morphogenetic signals in epithelial development and suggest a molecular mechanism for mesenchymal epithelial interactions.
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            Hepatocyte Growth Factor Up-Regulates MET Expression in Rat Fetal Hepatocytes in Primary Culture

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              • Abstract: not found
              • Article: not found

              Interleukin-6 induces proliferation of rat hepatocytes in vivo

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                Author and article information

                Journal
                EXN
                Nephron Exp Nephrol
                10.1159/issn.1660-2129
                Cardiorenal Medicine
                S. Karger AG
                1660-2129
                1998
                December 1998
                06 November 1998
                : 6
                : 6
                : 551-556
                Affiliations
                a Division of Nephrology and b Department of Internal Medicine, Universidade Estadual de Campinas, São Paulo, Brazil
                Article
                20570 Exp Nephrol 1998;6:551–556
                10.1159/000020570
                © 1998 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: 2, Tables: 3, References: 42, Pages: 6
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/20570
                Categories
                Original Paper

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