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Adeno-associated vi...
Adeno-associated viral vector-mediated expression of NT4-ADNF-9 fusion gene protects against aminoglycoside-induced auditory hair cell loss in vitro
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Zheng, Guoxi (författare)
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Zhu, Kang (författare)
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Wei, Junrong (författare)
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- Jin, Zhe (författare)
- Uppsala universitet,Fysiologi
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- Duan, Maoli (författare)
- Karolinska Institutet
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(creator_code:org_t)
- 2010-11-09
- 2011
- Engelska.
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Ingår i: Acta Oto-Laryngologica. - : Informa UK Limited. - 0001-6489 .- 1651-2251. ; 131:2, s. 136-141
- Relaterad länk:
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https://urn.kb.se/re...
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https://doi.org/10.3...
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http://kipublication...
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Abstract
Ämnesord
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- Conclusion: The present study suggests that adeno-associated viral vector AAV2-mediated expression of activity-dependent neurotrophic factor-9 (ADNF-9) in the cochlea could be a promising approach to protect the cochlea from aminoglycoside-induced impairment, although a further in vivo study is needed. Objectives: To construct vectors over-expressing ADNF-9 to overcome its short half-life and investigate the effect of ADNF-9 on aminoglycoside-induced hair cell impairment. Methods: We ligated ADNF-9 cDNA to the signal and leader peptides of neurotrophin 4 (NT4) and the fusion gene was named NT4-ADNF-9. NT4-ADNF-9 was subcloned into the prokaryotic expression vector pBV220 to obtain pBV220/NT4-ADNF-9. The induced recombinant ADNF-9 proteins were added into the dorsal root ganglia (DRG) cultures of embryonic day 8 chickens. In addition, we constructed the recombinant vector rAAV-NT4-ADNF-9 and transfected rat neonatal organ of Corti explants in the presence of aminoglycoside G418. Results: Our data showed that the induced expression of ADNF-9 protein could promote cultured DRG neuronal survival and neurite outgrowth. In addition, transfection of rAAV-NT4-ADNF-9 could prevent hair cell loss induced by G418 treatment in the rat organ of Corti.
Nyckelord
- Activity-dependent neurotrophic factor-9
- gene therapy
- neurotrophin 4
- sensorineural hearing loss
- MEDICINE
- MEDICIN
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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