Downregulation of Cav3.1 T-type Calcium Channel Expression in Age-related Hearing Loss Model
Downregulation of Cav3.1 T-type Calcium Channel Expression in Age-related Hearing Loss Model
复制标题
年龄相关性听力损失模型中 Cav3.1 T 型钙通道表达的下调
DOI：
10.1007/s11596-021-2416-0
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发表时间：
2021-08
影响因子：
2.4
通讯作者：
Sun Jin-wu
中科院分区：
文献类型：
--
作者：
Pan Chun-chen;Du Zhi-hui;Zhao Yi;Chu Han-qi;Sun Jin-wu
目的：老年性听力损失（阿勒）是世界范围内老年人最常见的感觉障碍，以耳蜗结构退化为特征。钙通道被认为有助于正常的听力。然而，T型电压激活钙通道Cav3.1在阿勒中的作用仍不清楚。在此，我们研究了Cav3.1在耳蜗和D-半乳糖诱导的衰老HEI-OC 1细胞中表达的年龄相关性变化。方法：对2月龄和12月龄C57 BL/6小鼠耳蜗进行评估。用D-半乳糖处理诱导耳科动物研究所Corti 1器官（HEI-OC 1）细胞衰老。采用免疫荧光技术研究Cav3.1在体内和体外的分布。结果：12月龄C57 BL/6小鼠与2月龄小鼠相比，毛细胞数量明显减少，听脑干阈值明显升高。Cav3.1主要定位于耳蜗毛细胞、螺旋神经节细胞和耳蜗侧壁，且Cav3.1蛋白和mRNA在老年耳蜗中的表达减少。结论：Cav3.1基因在耳蜗中的表达与AHL的发生有关，可能参与了阿勒的发病机制。
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.
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影响因子：
4.2
作者：
Rice RA;Berchtold NC;Cotman CW;Green KN
通讯作者：
Green KN
影响因子：
7.8
作者：
Wattamwar, Kapil;Qian, Z. Jason;Lalwani, Anil K.
通讯作者：
Lalwani, Anil K.
d-半乳糖诱导的耳蜗基底膜氧化应激和线粒体功能障碍：体外衰老模型
影响因子：
4.5
作者：
Guo, Bin;Guo, Qing;Gong, Shu-Sheng
通讯作者：
Gong, Shu-Sheng
影响因子：
2.5
作者：
Nie, Liping;Zhu, Jun;Yamoah, Ebenezer N.
通讯作者：
Yamoah, Ebenezer N.
影响因子：
2.9
作者：
Aguado C;García-Madrona S;Gil-Minguez M;Luján R
通讯作者：
Luján R