The analysis of molecular mechanism of Meniere disease based on the cellular stress response of endolymphatic sac cell
| Project/Area Number |
25861598
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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 | Nihon University |
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Principal Investigator |
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| Research Collaborator |
TSUCHIHASHI Nana
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 内耳 / 小胞体 / オートファジー / 内耳培養細胞 / 小胞体ストレス応答 / IP3R / LC3-II |
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| Outline of Final Research Achievements |
The cell viability after treatment of Tunicamycin was decreased in dose- and time- dependent manner. Ｗe defined this condition as the model of ER stress-induced auditory cell death. The findings that injured mitochondria surrounded by autophagosomes were confirmed under TEM. The expression of LC3-II was time-dependently increased in Tunicamycin-treated cells. These results mean that autophagy was consistently induced in Tunicamycin-treated cells. The expression of IP3R and CHOP was decreased after peaking at 12 hours after the treatment of Tunicamycin. The expression of BDNF and CAPS2 was time-dependently decreased in Tunicamycin-treated cells. The expression of Bcl-2 and Beclin1 was decreased in Tunicamycin-treated cells. The expression of Atoh1 and Myosin VIIA after treatment of Tunicamycin was time-dependently decreased. Our results lead to the suggestion that there is a signaling cross talk between ER stress response, IP3R activity through BDNF and autophagy in auditory cells.
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Report
(3 results)
Research Products
(3 results)
