Loss of Fascin2 increases susceptibility to cisplatin-induced hearing impairment and cochlear cell apoptosis in mice
Yan Wang1
Yingying Liu1
Yi Xie1
Jun Luan1
Rongrong Liu1
Yongjia Zhu1
Ying Ma1
Yi Fan1
Yan Sun2
Wenjing Shang1
Fengchan Han1
1.Department of Biochemistry and Molecular Biology,and Key Laboratory for Genetic Hearing Disorders in Shandong,Binzhou Medical University,346 Guanhai Road,Yantai,264003,Shandong,PR China2.Department of Otorhinolaryngology-Head and Neck Surgery,Affiliated Yantai Yuhuangding Hospital of Qingdao University,Yantai,264000,PR China
摘要：Objectives:Deletion of Fscn2 gene in mice has been linked to progressive hearing loss and degeneration of cochlear cells.Cisplatin,an antitumor drug,can cause various side effects,including ototoxicity.The aim of this study was to investigate the effects of Fscn2 on cisplatin-induced hearing impairment in mice and to explore the possible mechanism.
Methods:Two-week-old Fscn2+/+mice and Fscn2-/-mice were treated with two doses of cisplatin,with a 3-day recovery period in between.ABR(auditory evoked brain stem response)thresholds were measured and cochlear pathology was observed at 3 weeks of age.
Results:Both Fscn2+/+and Fscn2-/-mice showed hearing loss under the effect of cisplatin,but the impairment was more severe in Fscn2-/-mice.Further experiments showed that the percentages of outer hair cell(OHC)and spiral ganglion neuron(SGN)loss were significantly higher in cisplatin-treated Fscn2-/-mice compared to Fscn2+/+mice.Additionally,knockdown of Fscn2 in HEI-OC1 cells worsened cisplatin-induced cell apoptosis.Conclusion:FSCN2 mediates reduction of CDDP induced ototoxicity by inhibiting cell apoptosis.
机标关键词：apoptosiscisplatincellmicelosscochlearfascin2hearing
论文发表日期：2024-09-30
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：7( 133-139 )
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