| Project/Area Number |
12470527
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
応用薬理学・医療系薬学
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| Research Institution | Kumamoto University |
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Principal Investigator |
MIYATA Takeshi Kumamoto University, Graduate School of Pharmaceutical Sciences, Department of Chemico-Pharmacological Sciences, Professor, 大学院・医学薬学研究部, 教授 (90040310)
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| Co-Investigator(Kenkyū-buntansha) |
ISOHAMA Yoichiro Kumamoto University, Graduate School of Pharmaceutical Sciences, Department of Chemico-Pharmacological Sciences, Associate Professor, 大学院・医学薬学研究部, 助教授 (10240920)
KAI Hirofumi Kumamoto University, Graduate School of Pharmaceutical Sciences, Department of Molecular Medicine, Professor, 大学院・医学薬学研究部, 教授 (30194658)
TOKUTOMI Naofumi Kumamoto University, Graduate School of Medicine, Department of Pharmacology, Associate Professor, 大学院・医学薬学研究部, 助教授 (30227582)
FUKUNAGA Kohji Graduate School of Pharmaceutical Sciences, Tohoku University Department of Pharmacology, Professor, 大学院・薬学研究科, 教授 (90136721)
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| Project Period (FY) |
2000 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥13,200,000 (Direct Cost: ¥13,200,000)
Fiscal Year 2002: ¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2001: ¥4,100,000 (Direct Cost: ¥4,100,000)
Fiscal Year 2000: ¥5,500,000 (Direct Cost: ¥5,500,000)
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| Keywords | ETS transcription factor / airway mucin / GM-CSF / pulmonary surfactant / lung / epithelial cells / 気道上皮細胞 / 慢性閉塞性呼吸器疾患 / グリチルリチン / prostanlandin E_2 / 11β-hydroxysteroid dehydrogenase / 肺胞上皮細胞 / 細胞分化 / MEF / ETS-2 / 漢方薬 |
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| Research Abstract |
Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity in the world. However, there are only a few therapeutic drugs for the treatment of this disease. To evaluate new pharmacological approaches for COPD, it is necessary to make progress in understanding lung physiology and pathophysiology of COPD. The findings in this study were summarized below.
1. We have found that myeloid Elf-1 like factor (MEF) regulated the differentiation of airway epithelial cells. In addition to this, MEF-transfected carcinoma cells did not grow. Therefore, we proposed that MEF act as not only a differentiation regulator, but also a tumor suppressor.
2. We found that GM-CSF mRNA expression was upnregulated by ETS-2 transcription factor in adenocarcinoma cells, and was a target of protein kinase C.
3. We have found some new drugs to control mucous secretion in airway diseases. Among them, fudosteine, a new cysteine derivative, inhibited the formation of airway goblet cells, and glycyrrhizin, inhibited mucus production by enhancing the effect of glucocorticoids.
4. We have found new endogenous pulmonary surfactant secretagogues, adrenomedullin and prostaglandin E_2. We also found that there is a synergistic cross-talk between protein kinase A- and protein kinase C-dependent signalings in alveolar type II cells.
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