| Project/Area Number |
23659436
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Fukushima Medical University |
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Principal Investigator |
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| Project Period (FY) |
2011-04-28 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 間質性肺炎 / 網羅的遺伝子発現解析 / ミドカイン / midkine / IPF / BLM / BAL / 特発性肺線維症 / 網羅的遺伝子発現 / 遺伝子網羅解析 / 網羅的遺伝子解析 / 肺組織 / 肺癌 / 正常肺 |
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| Outline of Final Research Achievements |
Comprehensive gene expression analysis was done for mild fibrotic lung and normal lung and 25 genes which showed different expression levels were selected. These genes included several previously reported candidate genes for pulmonary fibrosis. Excluded these genes, Midkine (MDK) gene was selected one of the candidate gene and further precise analysis was done. Serum MDK levels were increased in patients with pulmonary fibrosis. In bronchoalveolar lavage fluid (BALF), MDK levels were reversely correlated with inflammatory cell counts. In mouse, intra-tracheal BLM induced fibrosis, and enhanced MDK-mRNA expression. In addition, stimulation of normal lung fibroblast by BLM increased MDK-mRNA expression. In MDK-KO mouse, protein levels in BALF were significantly decreased and correlated with lymphocyte percentage. TNF-a expression was also decreased. These results suggested that MDK is one of the molecule which modifies pathophysiology of pulmonary fibrosis.
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