| Project/Area Number |
26861420
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Otorhinolaryngology
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| Research Institution | Juntendo University |
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Principal Investigator |
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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 |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 遺伝性難聴 / GJB2 / コネキシン26 / 優性阻害変異 / プログラム細胞死 / アポトーシス / コルチ器 / トランスジェニックマウス / 先天性難聴 / 内耳コルチ器 / Greater epithelial ridge / GjB2遺伝子変異 / GJB2(コネキシン26変異)遺伝子変異 |
|---|
| Outline of Final Research Achievements |
The greater epithelial ridge (GER) is a developmental structure in the maturation of the organ of Corti. Situated near the inner hair cells of neonatal mice, the GER undergoes a wave of apoptosis after postnatal day 8 (P8). We evaluated the GER from P8 to P12 in transgenic mice that carry the R75W + mutation, a dominant-negative mutation of
human gap junction protein, beta 2, 26 kDa (GJB2) (also known as connexin 26 or CX26). In both non-transgenic (non-Tg) and R75W +mice, some GER cells exhibited apoptotic characteristics at P8. In the GER of non-Tg mice, both the total number of cells and the number of apoptotic cells decreased from P8 to P12. In contrast, apoptotic cells were still clearly evident in the GER of R75W +mice at P12. In R75W +mice, therefore, apoptosis in the GER persisted until a later stage of cochlear development.
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