| Project/Area Number |
15K09183
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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 | Yokohama City University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
金子 猛 横浜市立大学, 医学研究科, 教授 (90275066)
下川路 伊亮 横浜市立大学, 附属市民総合医療センター, 助教 (70751634)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
Fiscal Year 2015: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
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| Keywords | 気管支喘息 / 慢性閉塞性肺疾患 / IL-13 / TGFα / anoctamin-1 / CLCA-1 / 喘息・COPDオーバーラップ症候群 / NHBE / CLCA1 / 気道分泌制御 / MUC5AC / COPD / ACOS / TGF-α / ANO-1 / CXCL8 / 好中球エラスターゼ / ALI / SPDEF / STAT6 リン酸化 |
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| Outline of Final Research Achievements |
Compared with their counterparts with asthma or COPD alone, patients with ACO have significantly increased risk of exacerbations and worse respiratory symptoms. Activation of the interleukin-13 (IL-13) receptor leads to signal transducer and induction of chloride channel accessory 1 (CLCA1) and anoctamin-1(ANO1), increasing secretion of the gel-forming mucin MUC5AC. Activation of TGFα also leads to MUC5AC production via extracellular signal-regulated kinase (ERK1/2). We examined the effect of both IL-13 and TGFα signaling leading to mucin production. Histochemical analysis was performed using hematoxylin and eosin (HE) staining and MUC5AC immunostaining. MUC5AC, ANO1 and CLCA1 mRNA expression were evaluated by real-time PCR. Western analysis was used to assess phosphorylation. Our data suggest that the effect of both IL-13 and TGFα signaling increased mucus secretion perhaps via cross talk among cell-signaling transduction pathways.
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