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The role of the receptor for advanced glycation end-products in lung fibrosis

1 Department of Geriatric and Respiratory Medicine, Tohoku University School of Medicine, Sendai; and 2 Department of Biochemistry and Molecular Vascular Biology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan Submitted 26 February 2007 ; accepted in final form 15 October 20...

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Published in:American journal of physiology. Lung cellular and molecular physiology 2007-12, Vol.293 (6), p.L1427-L1436
Main Authors: He, Mei, Kubo, Hiroshi, Ishizawa, Kota, Hegab, Ahmed E, Yamamoto, Yasuhiko, Yamamoto, Hiroshi, Yamaya, Mutsuo
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container_title American journal of physiology. Lung cellular and molecular physiology
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Kubo, Hiroshi
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Yamamoto, Hiroshi
Yamaya, Mutsuo
description 1 Department of Geriatric and Respiratory Medicine, Tohoku University School of Medicine, Sendai; and 2 Department of Biochemistry and Molecular Vascular Biology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan Submitted 26 February 2007 ; accepted in final form 15 October 2007 The pathogenesis of pulmonary fibrosis remains unclear. The receptor for advanced glycation end-products (RAGE) is a multi-ligand receptor known to be involved in the process of fibrotic change in several organs, such as peritoneal fibrosis and kidney fibrosis. The aim of this study was to examine the contribution of RAGE during the acute inflammation and chronic fibrotic phases of lung injury induced by intratracheal instillation of bleomycin in mice. Bleomycin-induced lung fibrosis was evaluated in wild-type and RAGE-deficient (RAGE–/–) mice. Bleomycin administration to wild-type mice caused an initial pneumonitis that evolved into fibrosis. While RAGE–/– mice developed a similar early inflammatory response, the mice were largely protected from the late fibrotic effects of bleomycin. The protection afforded by RAGE deficiency was accompanied by reduced pulmonary levels of the potent RAGE-inducible profibrotic cytokines transforming growth factor (TGF)-β and PDGF. In addition, bleomycin administration induced high mobility group box 1 (HMGB-1) production, one of the ligands of RAGE, from inflammatory cells that accumulated within the air space. Coculture with HMGB-1 induced epithelial-mesenchymal transition (EMT) in alveolar type II epithelial cells from wild-type mice. However, alveolar type II epithelial cells derived from RAGE–/– mice did not respond to HMGB-1 treatment, such that the RAGE/HMGB-1 axis may play an important role in EMT. Also, bleomycin administration induced profibrotic cytokines TGF-β and PDGF only in wild-type mouse lungs. Our results suggested that RAGE contributes to bleomycin-induced lung fibrosis through EMT and profibrotic cytokine production. Thus, RAGE may be a new therapeutic target for pulmonary fibrosis. pulmonary fibrosis; alveolar type II epithelial cell; epithelial-mesenchymal transition; receptor for advanced glycation end-products; HMGB-1 Address for reprint requests and other correspondence: H. Kubo, Dept. of Geriatric and Respiratory Medicine, Tohoku Univ. School of Medicine, 1-1 Seiryoumachi, Aobaku, Sendai 980-8574, Japan (e-mail: hkubo{at}geriat.med.tohoku.ac.jp )
doi_str_mv 10.1152/ajplung.00075.2007
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The receptor for advanced glycation end-products (RAGE) is a multi-ligand receptor known to be involved in the process of fibrotic change in several organs, such as peritoneal fibrosis and kidney fibrosis. The aim of this study was to examine the contribution of RAGE during the acute inflammation and chronic fibrotic phases of lung injury induced by intratracheal instillation of bleomycin in mice. Bleomycin-induced lung fibrosis was evaluated in wild-type and RAGE-deficient (RAGE–/–) mice. Bleomycin administration to wild-type mice caused an initial pneumonitis that evolved into fibrosis. While RAGE–/– mice developed a similar early inflammatory response, the mice were largely protected from the late fibrotic effects of bleomycin. The protection afforded by RAGE deficiency was accompanied by reduced pulmonary levels of the potent RAGE-inducible profibrotic cytokines transforming growth factor (TGF)-β and PDGF. In addition, bleomycin administration induced high mobility group box 1 (HMGB-1) production, one of the ligands of RAGE, from inflammatory cells that accumulated within the air space. Coculture with HMGB-1 induced epithelial-mesenchymal transition (EMT) in alveolar type II epithelial cells from wild-type mice. However, alveolar type II epithelial cells derived from RAGE–/– mice did not respond to HMGB-1 treatment, such that the RAGE/HMGB-1 axis may play an important role in EMT. Also, bleomycin administration induced profibrotic cytokines TGF-β and PDGF only in wild-type mouse lungs. Our results suggested that RAGE contributes to bleomycin-induced lung fibrosis through EMT and profibrotic cytokine production. Thus, RAGE may be a new therapeutic target for pulmonary fibrosis. pulmonary fibrosis; alveolar type II epithelial cell; epithelial-mesenchymal transition; receptor for advanced glycation end-products; HMGB-1 Address for reprint requests and other correspondence: H. 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The aim of this study was to examine the contribution of RAGE during the acute inflammation and chronic fibrotic phases of lung injury induced by intratracheal instillation of bleomycin in mice. Bleomycin-induced lung fibrosis was evaluated in wild-type and RAGE-deficient (RAGE–/–) mice. Bleomycin administration to wild-type mice caused an initial pneumonitis that evolved into fibrosis. While RAGE–/– mice developed a similar early inflammatory response, the mice were largely protected from the late fibrotic effects of bleomycin. The protection afforded by RAGE deficiency was accompanied by reduced pulmonary levels of the potent RAGE-inducible profibrotic cytokines transforming growth factor (TGF)-β and PDGF. In addition, bleomycin administration induced high mobility group box 1 (HMGB-1) production, one of the ligands of RAGE, from inflammatory cells that accumulated within the air space. 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source American Physiological Society Free
subjects Animals
Apoptosis - drug effects
Bleomycin - administration & dosage
Blood Cell Count
Bronchoalveolar Lavage Fluid - cytology
Cell culture
Cell Differentiation - drug effects
Cell Membrane Permeability - drug effects
Cytokines
Epithelial Cells - drug effects
Epithelial Cells - pathology
HMGB1 Protein - metabolism
In Situ Nick-End Labeling
Lung - drug effects
Lung - pathology
Mesoderm - drug effects
Mesoderm - pathology
Mice
Mice, Inbred C57BL
Models, Biological
Platelet-Derived Growth Factor - metabolism
Pulmonary Fibrosis - chemically induced
Pulmonary Fibrosis - metabolism
Pulmonary Fibrosis - mortality
Pulmonary Fibrosis - pathology
Receptor for Advanced Glycation End Products
Receptors, Immunologic - deficiency
Receptors, Immunologic - metabolism
Respiratory diseases
Rodents
Studies
Survival Rate
Transforming Growth Factor beta1 - pharmacology
title The role of the receptor for advanced glycation end-products in lung fibrosis
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