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Published on: March 16, 2018
MiR-200c-3p affects cochlear hair cells damaged by oxidative stress via modulating Taok1 expression
Lihua Wu1,2,3, Ning Yang4, Qinghua Liu1
1Department of Otolaryngology, Head and Neck Surgery, Fujian Medical University ShengLi Clinical College, Fujian Provincial Hospital Fuzhou 350001, Fujian, China.
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.
Insights
MicroRNA-200c-3p protects cochlear hair cells from oxidative stress and apoptosis by targeting Taok1. This finding suggests miR-200c-3p as a potential therapeutic target for hearing loss.
Area of Science:
- Otolaryngology
- Molecular Biology
- Cell Biology
Background:
- Cochlear hair cell injury due to oxidative stress (OS) is a significant cause of hearing loss.
- Understanding the molecular mechanisms underlying this injury is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the role of miR-200c-3p in oxidative stress-induced cochlear hair cell injury.
- To elucidate the underlying molecular mechanisms involving Taok1.
Main Methods:
- HEI-OC1 cells were subjected to oxidative stress using tert-butyl hydroperoxide (t-BHP).
- miR-200c-3p expression, antioxidant enzyme levels (GSH-Px, SOD, CAT), MDA, Taok1, and apoptosis-related proteins were measured.
- Cell apoptosis was assessed using flow cytometry, and target validation was performed via dual luciferase reporter assay.
Main Results:
- Oxidative stress downregulated miR-200c-3p and upregulated Taok1 in HEI-OC1 cells, showing an inverse correlation.
- miR-200c-3p overexpression inhibited OS-induced apoptosis.
- Taok1 was identified as a direct target of miR-200c-3p, and its overexpression reversed the protective effects of miR-200c-3p.
Conclusions:
- miR-200c-3p suppresses oxidative stress and apoptosis in cochlear hair cells by targeting Taok1.
- miR-200c-3p represents a novel and potential therapeutic target for cochlear hair cell injury.
