Lihua Wu1,2,3, Ning Yang4, Qinghua Liu1, Yue Bai5, Bo Gao2. 1. Department of Otolaryngology, Head and Neck Surgery, Fujian Medical University ShengLi Clinical College, Fujian Provincial Hospital Fuzhou 350001, Fujian, China. 2. Department of Otolaryngology, Head and Neck Surgery, Institute of Otolaryngology, Chinese PLA General Hospital Beijing 100036, China. 3. Department of Otolaryngology, Head and Neck Surgery, Nanfang Hospital, Southern Medical Uiversity Guangzhou 510515, Guangdong, China. 4. Department of Otolaryngology, Head and Neck Surgery, First Affiliated Hospital of China Medical University Shenyang 110001, Liaoning, China. 5. Department of Ophthalmology, The First Affiliated Hospital of Fujian Medical University Fuzhou 350005, Fujian, China.
Abstract
OBJECTIVE: The aim of this study was to elucidate the role of miR-200c-3p in cochlear hair cells injured by oxidative stress (OS) and the underlying mechanisms. METHODS: The OS injury model of HEI-OC1 cells was induced by 100 μmol/L tert-butyl hydroperoxide (t-BHP). The expression of miR-200c-3p in HEI-OC1 was detected by RT-PCR, the levels of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), Catalase (CAT), and malondialdehyde (MDA) were determined with ELISA, and the expression levels of Taok1 and apoptosis-related proteins were measured by Western Blot. Flow cytometry was used to detect cell apoptosis. RESULTS: Real-time polymerase chain reaction (RT-qPCR) analysis identified down-regulated miR-200c-3p and up-regulated Taok1 in HEI-OC1 cells damaged by OS, as well as an inverse association between miR-200c-3p and Taok1. Cell tests confirmed that miR-200c-3p overexpression could effectively inhibit the OS response and apoptosis of HEI-OC1 cells. Bioinformatics prediction and dual luciferase reporter assay revealed that Taok1 was a direct target of miR-200c-3p. Taok1 overexpression could reverse the protective action of miR-200c-3p overexpression on the OS injury of HEI-OC1 cells. CONCLUSIONS: Given the capacity of miR-200c-3p to suppress the OS and apoptosis of HEI-OC1 cells via targeting Taok1, it can be a novel and potential therapeutic target for cochlear hair cell injury. AJTR
OBJECTIVE: The aim of this study was to elucidate the role of miR-200c-3p in cochlear hair cells injured by oxidative stress (OS) and the underlying mechanisms. METHODS: The OS injury model of HEI-OC1 cells was induced by 100 μmol/L tert-butyl hydroperoxide (t-BHP). The expression of miR-200c-3p in HEI-OC1 was detected by RT-PCR, the levels of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), Catalase (CAT), and malondialdehyde (MDA) were determined with ELISA, and the expression levels of Taok1 and apoptosis-related proteins were measured by Western Blot. Flow cytometry was used to detect cell apoptosis. RESULTS: Real-time polymerase chain reaction (RT-qPCR) analysis identified down-regulated miR-200c-3p and up-regulated Taok1 in HEI-OC1 cells damaged by OS, as well as an inverse association between miR-200c-3p and Taok1. Cell tests confirmed that miR-200c-3p overexpression could effectively inhibit the OS response and apoptosis of HEI-OC1 cells. Bioinformatics prediction and dual luciferase reporter assay revealed that Taok1 was a direct target of miR-200c-3p. Taok1 overexpression could reverse the protective action of miR-200c-3p overexpression on the OS injury of HEI-OC1 cells. CONCLUSIONS: Given the capacity of miR-200c-3p to suppress the OS and apoptosis of HEI-OC1 cells via targeting Taok1, it can be a novel and potential therapeutic target for cochlear hair cell injury. AJTR
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