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...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.展开更多
Age-related hearing loss (AHL), or presbycusis, is the most common neurodegenerative disorder and top communication deficit of the aged population. Genetic predisposition is one of the major factors in the development...Age-related hearing loss (AHL), or presbycusis, is the most common neurodegenerative disorder and top communication deficit of the aged population. Genetic predisposition is one of the major factors in the development of AHL. Generally, AHL is associated with an age-dependent loss of sensory hair cells, spiral ganglion neurons and stria vascularis cells in the inner ear. Although the mechanisms leading to genetic hearing loss are not completely understood, caspase-family proteases function as important signals in the inner ear pathology. It is now accepted that mouse models are the best tools to study the mechanism of genetic hearing loss or AHL. Here, we provide a brief review of recent studies on hearing improvement in mouse models of AHL by anti-apoptotic treatment.展开更多
基金supported by the National Natural Science Foundation of China(No.81771020,81570927 and 81271092)Grant for Scientific and Technological Development Plan for Medical and Health in Shandong Province(2019WS341).
文摘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.
基金supported by National Natural Science Foundation of China (No. 81271092, 81570927)Scientific and Technological Developing Grant in Shandong Province (2014GSF118083)+1 种基金Scientific and Technological Developing Grant for Medicine and Health in Shandong Province (2015WS0507)Research Initiation Grant of Binzhou Medical University (BY2012KYQD01, BY2013KYQD15)
文摘Age-related hearing loss (AHL), or presbycusis, is the most common neurodegenerative disorder and top communication deficit of the aged population. Genetic predisposition is one of the major factors in the development of AHL. Generally, AHL is associated with an age-dependent loss of sensory hair cells, spiral ganglion neurons and stria vascularis cells in the inner ear. Although the mechanisms leading to genetic hearing loss are not completely understood, caspase-family proteases function as important signals in the inner ear pathology. It is now accepted that mouse models are the best tools to study the mechanism of genetic hearing loss or AHL. Here, we provide a brief review of recent studies on hearing improvement in mouse models of AHL by anti-apoptotic treatment.
