| Project/Area Number |
20791212
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Otorhinolaryngology
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| Research Institution | Nagoya City University |
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Principal Investigator |
NAKAMURA Yoshihisa Nagoya City University, 大学院・医学研究科, 助教 (90360023)
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| Project Period (FY) |
2008 – 2009
|
| Project Status |
Completed (Fiscal Year 2009)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2009: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2008: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 杯細胞化生 / Math1 / TNF-α / レチノイン酸 / EGFR / Tnf-α / TNF・α |
|---|
| Research Abstract |
A key issue in otitis media (OM) is mucous cell metaplasia, a condition for hyperproduction of mucus in the middle ear mucosa and development of chronic OM. We demonstrated that Math1, a critical transcription factor for the development of mucous cells in the intestine, in the presence of pro-inflammatory cytokine (tumor necrotic factor alpha, TNF・) and retinoic acid (RA), promoted the differentiation of middle ear epithelial cells (MEECs) into mucus cells. RA strengthened the expression of Math1 via the epidermal growth factor receptor (EGFR) tyrosine kinase activity. A specific inhibitor for EGFR tyrosine kinase, AG1478, abrogated the Math1 expression and reduced mucus cell numbers. Math1 or EGFR tyrosine kinase should be the therapeutic molecular target for the OM.
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