HSV AMPLICON-MEDIATED NEUROTROPHIN-3 TRANSDUCTION PREVENTS MOUSE SPIRAL GANGLION NEURONS FROM DAMAGE
- VernacularTitle:HSV介导的神经营养因子-3体外表达拮抗顺铂的耳毒性作用
- Author:
Xiaowei CHEN
;
Keli CAO
;
- Publication Type:Journal Article
- Keywords:
Neurotrophin 3;
Cochlea;
Ototoxicity;
HSV amplicon
- From:
Acta Anatomica Sinica
2002;0(06):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To determine whether NT 3 overexpression could abrogate DDP toxicity in vitro . Methods We constructed a herpes simplex virus(HSV) amplicon vector to transduce a c myc tagged version of rat NT 3. In the HSVnt 3myc vector, the chimeric neurotrophin cDNA was placed under the transcriptional control of the CMVIE promoter. The resultant vector was packaged utilizing the recently developed helper virus free method. Results Transduction of NT 3myc in cultured mouse cochlear explants at a multiplicity of infection(MOI) of 0 25 resulted in production of NT 3 up to 3?g/L over a 48 hours period. The mouse cochlear explants were transduced with HSVnt 3myc or HSVmiap(control vector expressing the reporter gene, murine intestinal alkaline phosphatase) for 48 hours and the exposed to cisplatin for 48 hours.The cochlear explants transduced with HSVnt 3myc had a significantly greater number of SGN survival than the control group. NT 3 powerfully enhanced the process length and the density of SGNs.Conclusion These data demonstrate that the neurotrophic cDNA transduction via HSV amplicon helper free virus system can attenuate the ototoxic action of DDP on organotypic culture. The potency of NT 3 in protecting spiral ganglion neurons from degenerating suggests that neurotrophins might be useful for the prevention or treatment of hearing disorders. [
