1999 Fiscal Year Final Research Report Summary
Roles of PAF in bleomycin-induced pneumonia in knockout and transgenic mice
| 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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| Keywords | PAF / pulmonary fibrosis / bleomycin / transgenic mice / knockout mice |
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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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