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.
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.
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.
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.