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Involvement of calpain‐I and microRNA34 in kanamycin‐induced apoptosis of inner ear cells
Author(s) -
Yu Li,
Tang Hao,
Jiang Xiao Hua,
Tsang Lai Ling,
Chung Yiu Wa,
Chan Hsiao Chang
Publication year - 2010
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1042/cbi20100515
Subject(s) - spiral ganglion , calpain , ototoxicity , organ of corti , hair cell , inner ear , microbiology and biotechnology , apoptosis , programmed cell death , cochlea , kanamycin , annexin , biology , spiral ligament , neomycin , aminoglycoside , immunology , anatomy , antibiotics , biochemistry , genetics , chemotherapy , cisplatin , enzyme
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.