| Project/Area Number |
18K08146
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Review Section |
Basic Section 53030:Respiratory medicine-related
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| Research Institution | Oita University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
山末 まり 大分大学, 医学部, 講師 (40555174)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2023)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2020: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | 肺線維症 / サーファクタントタンパク質 / オステオポンチン |
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| Outline of Final Research Achievements |
We investigated the effect of loss of osteopontin function on the spontaneous development of pulmonary fibrosis in SftpcI73T knock-in mice, in which the main osteopontin-producing cells were macrophages and high concentrations of full-length and N-terminal osteopontin were detected in the lung lesion area. We generated SftpcI73T knock-in and Spp1 knock-out mice by crossing SftpcI73T knock-in mice with osteopontin (Spp1) knock-out mice. Loss of function of full-length osteopontin increased inflammatory cell infiltration and activation of cytokines and chemokines during the inflammatory phase. Osteopontin knockout did not improve lung fibrosis.
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| Academic Significance and Societal Importance of the Research Achievements |
今回の研究では，従来の報告と異なり，「オステオポンチンの機能喪失は，肺の炎症を増悪させ，肺線維化を改善しない」ことが明らかになり，本研究成果は，「オステオポンチンを治療ターゲットにするためには，オステオポンチンの機能喪失ではなく，オステオポンチンの機能調節が必要である」という学術的意義を持つ．さらに，本研究成果は，「オステオポンチン機能調節機能を，肺線維症の創薬に発展できる」という社会的意義を持つ．
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