| Project/Area Number |
10670534
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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 |
NAGASE Takahide The Univ. of Tokyo, Faculty of Medicine Lecturer, 医学部・附属病院, 講師 (40208004)
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| Co-Investigator(Kenkyū-buntansha) |
ISHII Satoshi Japan Society for the Promotion of Science, Researcher, 特別研究員 (10300815)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 1999: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1998: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | PAF / pulmonary fibrosis / bleomycin / transgenic mice / knockout mice / ブレオマイシン / 肺線維症 / 血小板治性化因子 / エイコサノイド |
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| Research Abstract |
Platelet-activating factor (PAF) is a proinflammatory phospholipid mediator that has various biological effects including cell adhesion, endothelial cell activation and the production of cytokines and eicosanoids via activation of G-protein-coupled PAF receptor (PAFR) . Considering its potent biological activity, PAF is potentially involved in the development of inflammatory disorders including interstitial pulmonary fibrosis.
The purpose of this report was to investigate the exact role of PAF in a murine model of bleomycin (BLM)-induced lung injury. To address this question, we used two different mutant mice established in our laboratory, i.e., 1) transgenic mice overexpressing the PAFR gene (PAFR-Tg) and controls (PAFR-Con), and 2) PAFR gene-disrupted mice (PAFR-KO) and controls (PAFR-WT).
We observed that overexpression of the PAFR gene seemed to exaggerate the acute lung injury induced by BLM, whereas disruption of the PAFR gene markedly attenuated the BLM-induced lung injury. These results indicate that the PAF receptor, and presumably PAF, may mediate important features of BLM-induced lung injury.
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