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首页> 外文期刊>Cell biology international. >Involvement of calpain-I and microRNA34 in kanamycin-induced apoptosis of inner ear cells.
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Involvement of calpain-I and microRNA34 in kanamycin-induced apoptosis of inner ear cells.

机译：钙蛋白酶I和microRNA34参与卡那霉素诱导的内耳细胞凋亡。

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摘要

Inner ear cells, including hair cells, spiral ganglion cells, stria vascularis cells and supporting cells on the basilar membrane, play a major role in transducing hearing signals and regulating inner ear homoeostasis. However, their functions are often damaged by antibiotic-induced ototoxicity. Apoptosis is probably involved in inner ear cell injury following aminoglycoside treatment. Calpain, a calcium-dependent protease, is essential for mediating and promoting cell death. We have therefore investigated the involvement of calpain in the molecular mechanism underlying ototoxicity induced by the antibiotic kanamycin in mice. Kanamycin (750 mg/kg) mainly induced cell death of cochlear cells, including stria vascularis cells, supporting cells and spiral ganglion cells, but not hair cells within the organ of Corti. Cell death due to apoptosis occurred in a time-dependent manner with concomitant up-regulation of calpain expression. Furthermore, the expression levels of two microRNAs, mir34a and mir34c, were altered in a dose-dependent manner in cochlear cells. These novel findings demonstrated the involvement of both calpain and microRNAs in antibiotic-induced ototoxicity.
机译：内耳细胞，包括毛细胞，螺旋神经节细胞，血管纹样细胞和基底膜上的支持细胞，在转导听力信号和调节内耳的稳态方面起着重要作用。然而，它们的功能经常被抗生素诱导的耳毒性所破坏。氨基糖苷类药物治疗后，凋亡可能与内耳细胞损伤有关。钙蛋白酶，一种钙依赖性蛋白酶，对于介导和促进细胞死亡至关重要。因此，我们研究了钙蛋白酶在小鼠卡那霉素诱导的耳毒性潜在分子机制中的作用。卡那霉素（750 mg / kg）主要诱导耳蜗细胞的细胞死亡，包括血管纹状细胞，支持细胞和螺旋神经节细胞，但不引起Corti器官内的毛细胞死亡。由于凋亡引起的细胞死亡以时间依赖性方式发生，同时伴有钙蛋白酶表达的上调。此外，在耳蜗细胞中，两种microRNA mir34a和mir34c的表达水平呈剂量依赖性变化。这些新颖的发现表明钙蛋白酶和microRNA都参与了抗生素诱导的耳毒性。

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