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      Intercellular Adhesion Molecule 1 Mediates Mononuclear Cell Infiltration into Rat Glomeruli after Renal Ablation

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          Abstract

          Mononuclear cells, primarily macrophages and lymphocytes, infiltrate the renal glomeruli and are involved in the progression of various glomerular diseases. Intercellular adhesion molecule 1 (ICAM-1) is expressed on the vascular endothelium and mediates the infiltration of leukocytes into the site of inflammation. Although the expression of ICAM-1 can be induced by the stimulation of inflammatory cytokine, ICAM-1 expression can also be induced by such nonimmune mechanisms as shear stress. Glomerular hyperfiltration is a major mechanism that contributes to the progression of the glomerular sclerosis that results from the loss of functioning nephrons. In the present study, we examined the role of ICAM-1 for mononuclear cell infiltration in the glomeruli of the five-sixth nephrectomized rat as a model of glomerular hyperfiltration. The fluorescence intensity score of the staining for ICAM-1 in the glomeruli of the five-sixth nephrectomized rats was significantly increased as compared with that in the control (sham-operated) rats at 1 week (1.51 ± 0.15 vs. 0.61 ± 0.13; p < 0.01) and 2 weeks (1.31 ± 0.17 vs. 0.51 ± 0.09; p < 0.01). The number of leukocytes present in the glomeruli was significantly increased in the five-sixth nephrectomized rats compared with control (sham-operated) rats at 1 week (3.44 ± 0.16 vs. 0.99 ± 0.08; p < 0.01) and 2 weeks (3.14 ± 0.14 vs. 0.89 ± 0.07; p < 0.01). Leukocytes mainly consisted of macrophages in the five-sixth nephrectomized rats at 1 week (2.39 ± 0.19) and 2 weeks (1.46 ± 0.11). Anti-ICAM-1 monoclonal antibody effectively prevented the infiltration of macrophages into the glomeruli following nephrectomy. These results indicate that glomerular hyperfiltration may be involved in the induction of the expression of ICAM-1 and the infiltration of macrophages into the renal glomeruli following glomerular injury.

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          Most cited references 2

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          Flow stimulates ICAM-1 expression time and shear stress dependently in cultured human endothelial cells.

           H Tsuboi,  J Ando,  A Kamiya (1995)
          Human umbilical vein endothelial cells were subjected to controlled levels of shear stress in a flow-loading apparatus, and changes in the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) were measured by flow cytometry. Application of shear stress (15 dynes/cm2) increased the cell surface expression of ICAM-1 2.7 times the control level 4 hr after the onset of flow, while it caused no change in VCAM-1 expression. The increase of ICAM-1 expression by shear stress was time- and force-dependent and reversible. Flow loading using perfusates with different viscosity revealed that the increase in ICAM-1 was shear-stress- rather than shear-rate-dependent. Reverse transcriptase/polymerase chain reaction analysis showed upregulation of ICAM-1 mRNA levels by shear stress, whose time course closely paralleled that of the cell surface protein. These results suggest that shear stress generated by blood flow acts as a regulator of cell adhesion molecule expression on vascular endothelial cells.
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            Shear stress increases heparin-binding epidermal growth factor-like growth factor mRNA levels in human vascular endothelial cells.

            Heparin-binding epidermal growth factor-like growth factor (HB-EGF) is a recently identified potent vascular smooth muscle cell (SMC) mitogen. We investigated the effect of shear stress on human HB-EGF mRNA levels in cultured human umbilical vein endothelial cells (HUVEC). In response to shear stress (8 dyne/cm2), HB-EGF mRNA levels in HUVEC increased rapidly, peaked at 3 h, and returned to near base line at 7 h. The shear stress-induced HB-EGF gene expression in HUVEC is completely blocked by 12-O-tetra-decanoylphorbol-13-acetate pre-treatment, suggesting the induction of HB-EGF is mediated by protein kinase C.
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              Author and article information

              Journal
              NEF
              Nephron
              10.1159/issn.1660-8151
              Nephron
              S. Karger AG
              1660-8151
              2235-3186
              1998
              May 1998
              29 April 1998
              : 79
              : 1
              : 91-98
              Affiliations
              a Department of Medicine III, Okayama University Medical School, Okayama, and b Department of Bioregulation, Biomedical Research Center, Osaka University Medical School, Osaka, Japan
              Article
              44997 Nephron 1998;79:91–98
              10.1159/000044997
              9609468
              © 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: 6, References: 41, Pages: 8
              Product
              Self URI (application/pdf): https://www.karger.com/Article/Pdf/44997
              Categories
              Original Paper

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