| Project/Area Number |
21791647
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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 | Juntendo University |
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Principal Investigator |
IIZUKA Takasi Juntendo University, 医学部, 助教 (40372932)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 難聴モデルマウス / 遺伝子導入 / ウイルスベクター / 遺伝子治療 / 難聴治療 / モデルマウス |
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| Research Abstract |
Hereditary deafness affects about 1 in 2,000 children and mutations in the GJB2 gene are the major cause in various ethnic groups. In order to establish the fundamental therapy of congenital deafness, we generated targeted disruption of Gjb2 using Cre recombinase controlled by P0. Using this animal model, we examined the potential of gene therapy in the inner ear, using the homozygous mutant mice and the heterozygous mutant mice. Adeno-associated virus (AAV) vectors carrying the gap junction beta 2 protein (Gjb2) gene were injected into the scala tympani through the round window of the cochlea of the homozygous mutant adult mice. The expression of Cx26 was not seen in the supporting cells and the hearing ability was not improved.
We succeeded in gene introduction to the supporting cells of neonatal mice without hearing loss using adeno-associated virus vectors. We are going to introduce this virus into the Gjb2 knockout mouse in future to cure hereditary deafness.
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