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大鼠卡那霉素耳中毒后耳蜗TMPRSS3蛋白的表达 被引量：1

Expression of TMPRSS3 in the rat cochlea following kanamycin ototoxicity
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摘要 目的:建立氨基甙类抗生素(aminoglycoside antibiotics,AmAn)致聋动物模型,观察内耳跨膜丝氨酸蛋白酶3(transmembrane protease,serine 3,TMPRSS3)的表达变化,探讨其在AmAn致聋中的作用机制。方法:选取健康SD大鼠40只,随机分为4组:对照组、硫酸卡那霉素3日组、硫酸卡那霉素7日组、硫酸卡那霉素14日组(n=10)。建立AmAn致聋动物模型,以听觉脑干反应(ABR)阈值作为评价听功能指标,采用免疫组织化学、Western印迹分析AmAn致聋后耳蜗TMPRSS3蛋白表达的变化。结果:成功建立了AmAn致聋动物模型,随着卡那霉素注射时间延长,大鼠ABR阈值逐渐升高,耳蜗TMPRSS3蛋白表达水平逐渐降低,与对照组比较,差异有统计学意义(P<0.01)。结论:蛋白酶TMPRSS3对于正常听觉功能维护起重要作用,它参与了AmAn致聋过程,其表达水平下调可能是AmAn耳毒性发生机制中的一个重要环节。 Objective To establish the kanamycin-induced deafness model in SD rats,and to investigate the expression and significance of transmembrane protease,serine 3（TMPRSS3） in the cochlea following kanamycin ototoxicity.Methods A total of 40 male SD rats were randomly divided into 4 groups.The experimental rats received intramuscular kanamycin sulfate for 3,7,and 14 consecutive days,and the control group were treated with normal saline for 14 days.Auditory brainstem responses（ABR） were obtained before and after the kanamycin administration.The expression of TMPRSS3 in the cochlea was identified and detected by immunohistochemistry and Western blot.Results Kanamycin-induced deafness model in the SD rats was successfully established.ABR thresholds were increased and the expression of TMPRSS3 in the cochlea was reduced after the kanamycin injection（P0.01）.Conclusion TMPRSS3 may play an important role in normal cochlea function and involve in the process of aminoglycoside antibiotics induced deafness.
作者 彭安全 葛圣雷 汪芹 谢鼎华 伍伟景 肖自安
机构地区 中南大学湘雅二医院耳鼻咽喉头颈外科 中南大学耳科研究所
出处 《中南大学学报（医学版）》 CAS CSCD 北大核心 2011年第10期987-991,共5页 Journal of Central South University ：Medical Science
基金 国家自然科学基金(30700940)~~
关键词 跨膜丝氨酸蛋白酶3 硫酸卡那霉素 耳蜗 耳毒性 transmembrane protease serine 3 kanamycin cochlea ototoxicity
分类号 R764 [医药卫生—耳鼻咽喉科]
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参考文献16

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二级参考文献26

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共引文献1

同被引文献11

  • 1苗英章,张勋,李秀霞,张培俭,杨更森,孙捷英.老年人听觉功能个体差异的ECochG和ABR研究[J].中国耳鼻咽喉颅底外科杂志,1996,2(4):201-203. 被引量：6
  • 2Scott HS, Kudoh J, Wattenhofer M, et al. Insertion of beta- satellite repeats identifies a transmembrane protease causing both congenital and childhood onset aut0somal recessive deafness [J]. Nat Genet, 2001, 27(1): 59-63.
  • 3Weegerink NJ, Schraders M, Oostrik J, et al. Genotype-phe- notype correlation in DFNB8/10 families with TMPRSS3 muta- tions[J]. J Assoc Res Otolaryngol, 2011, 12(6) : 753 - 766.
  • 4Wattenhofer M, Di Iorio MV, Rabionet R, et al. Mutations in the TMPRSS3 gene are a rare cause of childhood nonsyndromic deafness in Caucasian patients [ J ] . J Mol Med, 2002 , 80(2): 124-131.
  • 5Lee Y J, Park D, Kim SY, et al. Pathogenic mutations but not polymorphisms in congenital and childhood onset autosomal recessive deafness disrupt the pmteolytic activity of TMPRSS3 [J]. J Med Genet, 2003, 40(8) : 629 -631.
  • 6Wattenhofer M, Sahin-Calapoglu N, Andreasen D, et al. A novel TMPRSS3 missense mutation in a DFNB8/10 family pre- vents proteolytic activation of the protein [ J ]. Hum Genet, 2005, 117(6) : 528 -535.
  • 7Guipponi M, Tan J, Ping ZFC, et al. Mice deficient for the type II transmembrane serine pmtease, TMPRSS1/hepsin, ex- hibit profound hearing loss [ J ]. Am J Pathol, 2007, 171 (2): 608 -616.
  • 8Guipponi M, Toh MY, Tan J, et al. An integrated genetic and functional analysis of the role of type II transmembrane ser- ine proteases ( TMPRSSs ) in heating loss [ J ]. Hum Mutat, 2008, 29(1): 130-141.
  • 9Guipponi M, Vuagniaux G, Wattenhofer M, et al. The trans- membrane serine protease ( TMPRSS3 ) mutated indeafness DFNB8! 10 activates the epithelial sodium channel (ENaC) in vitro [ J]. Hum Mol Genet, 2002, 11 (23) : 2829 - 2836.
  • 10Guipponi M, Antonarakis SE, Scott HS. TMPRSS3, a type lI transmembrane serine protease mutated in non-syndromic autosomal recessive deafness [ J ]. Front Biosci, 2008, 1 (13): 1557-1567.

引证文献1

中南大学学报（医学版）
2011年 第10期

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