| Project/Area Number |
26462562
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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 |
Otorhinolaryngology
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| Research Institution | Nagoya City University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
鈴木 元彦 名古屋市立大学, 大学院医学研究科, 准教授 (50326138)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2015: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000)
Fiscal Year 2014: ¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
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| Keywords | Math1 / TNF-α / レチノイン酸 / 杯細胞化生 / 中耳炎 / 慢性中耳炎 / GFI1 / SPDEF / AGR2 / Clca1 / Gcnt3 |
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| Outline of Final Research Achievements |
A key issue in otitis media (OM) is mucous cell metaplasia in the middle ear mucosa, a condition for hyperproduction of mucus in the middle ear mucosa and development of chronic OM. We demonstrated that Math1 significantly increased the mucus-like cell numbers in the middle ear mucosa of mice. Math1, in the presence of TNF-a and retinoic acid (RA), synergistically promoted the differentiation of mouse middle ear epithelial cells (mMEEC) into mucus-like cells via upregulation of mucins and their chaperones:trefoil factors (TFFs) in vitro. We also demonstrated that Math1 activation (translocation to nucleus) was inhibited by epidermal growth factor receptor tyrosine kinase inhibitor, AG1478. In addition, mucous cell metaplasia induced by TNFα and RA was abrogated by AG1478. These results suggested that regulation of Math1 could prevent mucous cell metaplasia in chronic otitis media.
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