Downregulation of Cav3.1 T-type Calcium Channel Expression in Age-related Hearing Loss Model  

作　　者：Chun-chen PAN Zhi-hui DU Yi ZHAO Han-qi CHU Jin-wu SUN 

机构地区：[1]Department of Otorhinolaryngology-Head and Neck Surgery,the First Affiliated Hospital of University of Science and Technology of China,Division of Life Sciences and Medicine,University of Science and Technology of China,Hefei,230001,China [2]Department of Otolaryngology-Head and Neck Surgery,Tongji Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan,430030,China

出　　处：《Current Medical Science》2021年第4期680-686,共7页当代医学科学（英文）

基　　金：supported by grants from the National Natural Sciences Foundation of China(No.81800911 and No.81771004);the Anhui Natural Science Foundation(No.1808085QH248);Fundamental Research Funds for the Central Universities(No.WK9110000053).

摘　　要：Objective Age-related hearing loss(AHL),characterized by degeneration of cochlea structures,is the most common sensory disorder among the elderly worldwide.The calcium channel is considered to contribute to normal hearing.However,the role of the T-type voltage-activated calcium channel,Cav3.1,remains unclear in AHL.Here,we investigate the age-related change of Cav3.1 expression in the cochlea and D-gal-induced senescent HEI-OC1 cells.Methods Cochleae from C57BL/6 mice at 2 months and 12 months of age were assessed.Senescence in House Ear Institute-Organ of Corti 1(HEI-OC1)cells was induced by D-gal treatment.The immunofluorescence technique was employed to investigate the distribution of Cav3.1 in vivo and in vitro.Quantitative assessment was achieved by Western blotting and real-time PCR.Results In comparison with 2-month-old animals,12-month old C57BL/6 mice exhibited great loss of hair cells and elevated auditory brainstem threshold.The Cav3.1 was located in hair cells,spiral ganglion cells,lateral walls,and the expression of Cav3.1 protein and mRNA decreased in the aged cochleae.D-gal-induced senescence assay confirmed the down-regulation of Cav3.1 expression in senescent HEI-OC1 cells.Conclusion Our results show that age-related down-regulated expression of Cav3.1 in the cochleae is associated with AHL and may contribute to the pathogenesis of AHL.

关 键 词：PRESBYCUSIS HEI-OC1 COCHLEA C57BL/6 mouse 

分 类 号：R73[医药卫生—肿瘤]