The influence of transferred ubxiap on the progression of age-related hearing loss in C57BL/6J mice.

摘要

Presbycusis is a predominant neurodegenerative disease of aging, in which apoptosis has been shown to be heavily involved. In this study, we evaluated if presbycusis can be delayed by over-expression of the X-linked Inhibitor of Apoptosis Protein (XIAP), which was tagged with 6-myc (Myc-XIAP) through genetic manipulation in a mouse model. Hearing loss with age was evaluated chronologically by auditory brainstem responses and was found to develop much slower in the transgenic group in which XIAP was over-expressed than in the wild-type controls. Cochlear hair cell loss was also found to be significantly reduced in the transgenic group. Western blot revealed increased endogenous XIAP levels with age in the cochlea but not in the brain, suggesting an increased activation of apoptosis with age in the cochleae. The Myc-XIAP level remained stable in both tissues with age. There was no difference in endo-XIAP levels across genotype.