| Project/Area Number |
23591165
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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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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Kanazawa Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
IGUCHI Masaharu 金沢医科大学, 医学部, 助教 (60350758)
KOBAYASHI Makoto 金沢医科大学, 医学部, 助教 (20460355)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 間質性肺炎 / 肺サーファクタント / 細胞内輸送 / 肺胞上皮細胞 / ヘルマンスキー・パドラック症候群 / Ｒａｂ３８低分子量Ｇタンパク質 / ヘルマンスキーパドラック症候群 / 肺胞ＩＩ型上皮細胞 / 肺胞II型上皮細胞 / 細胞内輸送異常 |
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| Research Abstract |
To investigate pathogenesis of interstitial pneumonia that is caused by perturbation of lung surfactant transport, we analyzed the lungs of Long Evans Cinnamon rats, an animal model of Hermansky-Pudlak syndrome. There were remarkably enlarged giant lamellar bodies and increased lung surfactant in alveolar type II cells. Basal secretion of surfactant from the cells was inhibited but agonist-induced secretion was reversely enhanced. Adenovector-mediated delivery of Rab38 ameliorated these surfactant abnormalities. Unexpectedly, the rat lungs showed emphysematous changes. It is suspected that complication with infection, air pollution, and/or aging would be necessary in addition to a primary genetic abnormality to develop interstitial pneumonia in the disease.
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