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Title: Oncostatin M induces upregulation of claudin-2 in rodent hepatocytes coinciding with changes in morphology and function of tight junctions

Abstract

In rodent livers, integral tight junction (TJ) proteins claudin-1, -2, -3, -5 and -14 are detected and play crucial roles in the barrier to keep bile in bile canaculi away from the blood circulation. Claudin-2 shows a lobular gradient increasing from periportal to pericentral hepatocytes, whereas claudin-1 and -3 are expressed in the whole liver lobule. Although claudin-2 expression induces cation-selective channels in tight junctions of epithelial cells, the physiological functions and regulation of claudin-2 in hepatocytes remain unclear. Oncostatin M (OSM) is a multifunctional cytokine implicated in the differentiation of hepatocytes that induces formation of E-cadherin-based adherens junctions in fetal hepatocytes. In this study, we examined whether OSM could induce expression and function of claudin-2 in rodent hepatocytes, immortalized mouse and primary cultured proliferative rat hepatocytes. In the immortalized mouse and primary cultured proliferative rat hepatocytes, treatment with OSM markedly increased mRNA and protein of claudin-2 together with formation of developed networks of TJ strands. The increase of claudin-2 enhanced the paracellular barrier function which depended on molecular size. The increase of claudin-2 expression induced by OSM in rodent hepatocytes was regulated through distinct signaling pathways including PKC. These results suggest that expression of claudin-2 in rodent hepatocytes maymore » play a specific role as controlling the size of paracellular permeability in the barrier to keep bile in bile canaculi.« less

Authors:
 [1];  [2];  [3];  [4];  [1];  [2];  [4];  [4];  [4];  [1];  [4]
  1. Department of Surgery, Sapporo Medical University School of Medicine, Sapporo (Japan)
  2. (Japan)
  3. Department of Pathology, Sapporo Medical University School of Medicine, S1. W17. Sapporo 060-8556 (Japan). E-mail: ktakashi@sapmed.ac.jp
  4. Department of Pathology, Sapporo Medical University School of Medicine, S1. W17. Sapporo 060-8556 (Japan)
Publication Date:
OSTI Identifier:
20972158
Resource Type:
Journal Article
Resource Relation:
Journal Name: Experimental Cell Research; Journal Volume: 313; Journal Issue: 9; Other Information: DOI: 10.1016/j.yexcr.2007.03.010; PII: S0014-4827(07)00125-5; Copyright (c) 2007 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA)
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; BILE; BLOOD CIRCULATION; LIVER; LIVER CELLS; MICE; MORPHOLOGY; PERMEABILITY; PROTEINS; RATS

Citation Formats

Imamura, Masafumi, Department of Pathology, Sapporo Medical University School of Medicine, S1. W17. Sapporo 060-8556, Kojima, Takashi, Lan, Mengdong, Son, Seiichi, Department of Pathology, Sapporo Medical University School of Medicine, S1. W17. Sapporo 060-8556, Murata, Masaki, Osanai, Makoto, Chiba, Hideki, Hirata, Koichi, and Sawada, Norimasa. Oncostatin M induces upregulation of claudin-2 in rodent hepatocytes coinciding with changes in morphology and function of tight junctions. United States: N. p., 2007. Web. doi:10.1016/j.yexcr.2007.03.010.
Imamura, Masafumi, Department of Pathology, Sapporo Medical University School of Medicine, S1. W17. Sapporo 060-8556, Kojima, Takashi, Lan, Mengdong, Son, Seiichi, Department of Pathology, Sapporo Medical University School of Medicine, S1. W17. Sapporo 060-8556, Murata, Masaki, Osanai, Makoto, Chiba, Hideki, Hirata, Koichi, & Sawada, Norimasa. Oncostatin M induces upregulation of claudin-2 in rodent hepatocytes coinciding with changes in morphology and function of tight junctions. United States. doi:10.1016/j.yexcr.2007.03.010.
Imamura, Masafumi, Department of Pathology, Sapporo Medical University School of Medicine, S1. W17. Sapporo 060-8556, Kojima, Takashi, Lan, Mengdong, Son, Seiichi, Department of Pathology, Sapporo Medical University School of Medicine, S1. W17. Sapporo 060-8556, Murata, Masaki, Osanai, Makoto, Chiba, Hideki, Hirata, Koichi, and Sawada, Norimasa. Tue . "Oncostatin M induces upregulation of claudin-2 in rodent hepatocytes coinciding with changes in morphology and function of tight junctions". United States. doi:10.1016/j.yexcr.2007.03.010.
@article{osti_20972158,
title = {Oncostatin M induces upregulation of claudin-2 in rodent hepatocytes coinciding with changes in morphology and function of tight junctions},
author = {Imamura, Masafumi and Department of Pathology, Sapporo Medical University School of Medicine, S1. W17. Sapporo 060-8556 and Kojima, Takashi and Lan, Mengdong and Son, Seiichi and Department of Pathology, Sapporo Medical University School of Medicine, S1. W17. Sapporo 060-8556 and Murata, Masaki and Osanai, Makoto and Chiba, Hideki and Hirata, Koichi and Sawada, Norimasa},
abstractNote = {In rodent livers, integral tight junction (TJ) proteins claudin-1, -2, -3, -5 and -14 are detected and play crucial roles in the barrier to keep bile in bile canaculi away from the blood circulation. Claudin-2 shows a lobular gradient increasing from periportal to pericentral hepatocytes, whereas claudin-1 and -3 are expressed in the whole liver lobule. Although claudin-2 expression induces cation-selective channels in tight junctions of epithelial cells, the physiological functions and regulation of claudin-2 in hepatocytes remain unclear. Oncostatin M (OSM) is a multifunctional cytokine implicated in the differentiation of hepatocytes that induces formation of E-cadherin-based adherens junctions in fetal hepatocytes. In this study, we examined whether OSM could induce expression and function of claudin-2 in rodent hepatocytes, immortalized mouse and primary cultured proliferative rat hepatocytes. In the immortalized mouse and primary cultured proliferative rat hepatocytes, treatment with OSM markedly increased mRNA and protein of claudin-2 together with formation of developed networks of TJ strands. The increase of claudin-2 enhanced the paracellular barrier function which depended on molecular size. The increase of claudin-2 expression induced by OSM in rodent hepatocytes was regulated through distinct signaling pathways including PKC. These results suggest that expression of claudin-2 in rodent hepatocytes may play a specific role as controlling the size of paracellular permeability in the barrier to keep bile in bile canaculi.},
doi = {10.1016/j.yexcr.2007.03.010},
journal = {Experimental Cell Research},
number = 9,
volume = 313,
place = {United States},
year = {Tue May 15 00:00:00 EDT 2007},
month = {Tue May 15 00:00:00 EDT 2007}
}