| Project/Area Number |
23592490
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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 |
NAKAMURA Yoshihisa 名古屋市立大学, 医学(系)研究科(研究院), 助教 (90360023)
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| Co-Investigator(Kenkyū-buntansha) |
SUZUKI Motohiko 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) |
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: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2011: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
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| Keywords | 杯細胞化生 / Math1 / TNFα / レチノイン酸 / EGFR / TNF-α / 杯細分化 |
|---|
| Research Abstract |
We demonstrated that Math1, a critical transcription factor for the development of mucous cells in the intestine, significantly increased the mucus-like cell numbers in the middle ear mucosa of mice. Math1, in the presence of pro-inflammatory cytokine (TNFa) and epithelial differentiation factor retinoic acid (RA), synergistically promoted the differentiation of mouse middle ear epithelial cells 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 TNFa 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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