2003 Fiscal Year Final Research Report Summary
Roles of CGRP family peptides in the molecular mechanisms underlying bronchial asthma: the development of novel therapeutic approach
| Project/Area Number |
14570544
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | The University of Tokyo |
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Principal Investigator |
YAMAMOTO Hiroshi The Univ. of Tokyo, Faculty of Medicine, Research Associate, 医学部附属病院, 助手 (10361487)
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| Co-Investigator(Kenkyū-buntansha) |
TOMIYA Tetsuji The Univ. of Tokyo, Faculty of Medicine, Research Associate, 医学部附属病院, 教務職員 (50345203)
SHINDO Takayuki The Univ. of Tokyo, Faculty of Medicine, Research Associate, 医学部附属病院, 助手 (90345215)
NAGASE Takahide The Univ. of Tokyo, Faculty of Medicine, Professor, 医学部附属病院, 教授 (40208004)
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| Project Period (FY) |
2002 – 2003
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| Keywords | CGRP / Bronchial asthma / Airway heperresponsiveness / Knockout mouse |
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| Research Abstract |
Bronchial hyperresponsiveness and eosinophilia are major characteristics of asthma. Calcitonin gene-related peptide (CGRP) is a neuropeptide that has various biological actions. In the current study, we questioned whether CGRP might have pathophysiological roles in airway hyperresponsiveness and eosinophilia in asthma. To determine the exact roles of endogenous CGRP in vivo, we chose to study antigen-induced airway responses using CGRP gene-disrupted mice. After ovalbumin sensitization and antigen challenge, we assessed airway responsiveness and measured proinflammatory mediators. In the sensitized CGRP gene-disrupted mice, antigen-induced bronchial hyperresponsiveness was significantly attenuated compared to the sensitized wild type mice. Antigen challenge induced eosinophil infiltration in bronchoalveolar lavage fluid (BALF), whereas no differences were observed between the wild type and CGRP mutant mice. Antigen-induced increases in cysteinyl leukotriene production in the lung was significantly reduced in the CGRP-disrupted mice. These findings suggest that CGRP could be involved in the antigen-induced airway hyperresponsiveness, but not eosinophil infiltration, in mice. The CGRP mutant mice may provide appropriate models to study molecular mechanisms underlying CGRP-related diseases.
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[Publications] Aoki-Nagase T, Nagase T, Oh-hashi Y, Shindo T, Kurihara Y, Yamaguchi Y, Yamamoto H, Tomita T, Ohga E, Nagai R, Kurihara H, Ouchi Y.: "Attenuation of antigen-induced airway hyperresponsiveness in CGRP-deficient mice."Am J Physiol Lung Cell Mol Physiol. 283. L963-L970 (2002)
Description
「研究成果報告書概要(和文)」より
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[Publications] Nagase T, Uozumi N, Aoki-Nagase T, Terawaki K, Ishii S, Tomita T, Yamamoto H, Hashizume K, Ouchi Y, Shimizu T.: "A potent inhibitor of cytosolic phospholipase A_2, arachidonyl trifluoromethyl ketone, attenuates LPS-induced lung injury in mice"Am J Physiol Lung Cell Mol Physiol. 284. L720-L726 (2003)
Description
「研究成果報告書概要(和文)」より
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[Publications] Aoki-Nagase T, Nagase T, Oh-hashi Y, Shindo T, Kurihara Y, Yamaguchi Y, Yamamoto H, Tomita T, Ohga E, Nagai R, Kurihara H, Ouchi Y.: "Attenuation of antigen-induced airway hyperresponsiveness in CGRP-deficient mice."Am J Physiol Lung Cell Mol Physiol. 283. L963-L970 (2002)
Description
「研究成果報告書概要(欧文)」より
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[Publications] Nagase T, Uozumi N, Aoki-Nagase T, Terawaki K, Ishii S, Tomita T, Yamamoto H, Hashizume K, Ouchi Y, Shimizu T.: "A potent inhibitor of cytosolic phospholipase A_2, arachidonyl trifluoromethyl ketone, attenuates LPS-induced lung injury in mice."Am J Physiol Lung Cell Mol Physiol. 284. L720-L726 (2003)
Description
「研究成果報告書概要(欧文)」より
