Smad5基因缺陷导致小鼠听力重度损失  

The mutation in Smad5 genes lead to severe hearing loss in mouse

作　　者：郭维[1] 杨仕明[1] 刘清明[1] 孙彦询[2] 杨晓[2] 韩东一[1] 杨伟炎[1] 

机构地区：[1]解放军耳鼻咽喉研究所,解放军总医院耳鼻咽喉-头颈外科,北京100853 [2]军事医学科学院生物工程研究所发育和疾病遗传学研究室,北京100071

出　　处：《中华耳科学杂志》2006年第3期190-193,共4页Chinese Journal of Otology

基　　金：国家自然科学基金(30000189;30571017);军队"十五"科研基金(01Q050);北京市自然科学基金(7042061)资助

摘　　要：目的观察Smad5基因敲除小鼠听功能的变化及其特点。方法50只Smad5基因敲除的杂合子小鼠与25只野生型小鼠分成5组:2周、4周、8周、12周、24周组。分别行脑干诱发电位(ABR)检测,刺激声用click及toneburst(8kHz,16kHz,32kHz)。结果Smad5基因敲除杂合子小鼠2周、4周、8周、12周、24周click刺激ABR平均听阈分别为93±2.78dBSPL;38.7±2.58dBSPL;64.8±3.78dBSPL;81.5±2.48dBSPL;95.7±4.78dBSPL。野生型小鼠平均听阈分别为99±2.78dBSPL;38±3.65dBSPL;32±1.78dBSPL;32±2.70dBSPL;47±5.78dBSPL。经统计学处理,除2周和4周组P>0.05两者听阈差异无显著性外,其他时间段P<0.01,说明基因敲除小鼠与野生型小鼠听阈差异有显著性。toneburst(8kHz,16kHz,32kHz)结果与click刺激ABR听阈结果基本一致。结论Smad5基因敲除导致小鼠随月龄增加而听力损失加重。Objective To observe the change and characteristic in auditory physiology of the heterozygote Smad5 knockout mouse. Methods Fifty heterozygote Smad5 knockout mice at 2, 4, 8, 12 and 24 weeks and 25 wild type mice at the same ages （n = 5 for each group） were evaluated by auditory brainstem response （ABR）. Two different sound stimuli, click and tone burst, were performed. Results ABR thresholds for the heterozygote Smad5 knockout mice at 2, 4, 8, 12 and 24 weeks were 93 ± 2.78 dB SPL, 38.7 ± 2.58 dB SPL, 64.8 ± 3.78 dB SPL, 81.5 ± 2.48 dB SPL, 95.7±4.78 dB SPL. In contrast the ABR thresholds for the wild mice were 99 ± 2.78 dB SPL, 38 ± 3.65 dB SPL, 32 ± 1.78 dB SPL, 32 ± 2.70 dB SPL, 47 ± 5.78 dB SPL. The ABR thresholds had no significant differentce （P 〉 0.05） between the Smad5 knockout mice and the wild type mice at 2 and 4 weeks. But the ABR thresholds at 8, 12, and 24 weeks were statistically significant different （P 〈 0.01 ）. The ABR thresholds for tone burst stimuli were similar to the result from the click stimuli in high frequencies. Conclusion Smad5 knockout lead to a severe hearing loss in the mouse.

关 键 词：SMAD5 小鼠 基因敲除 听力损失 

分 类 号：R394.112[医药卫生—医学遗传学] R339.16[医药卫生—基础医学]