ArticleScientific reports2016
Reduced TRMU expression increases the sensitivity of hair-cell-like HEI-OC-1 cells to neomycin damage in vitro.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 51 citations in OpenAlex.
- Targeting Sensory Neuropathies Through Neurotrophin-Based Approaches.Cellular and molecular neurobiology · 2026Review
- TRMU Confers Resistance of Melanoma Cells to Vemurafenib through Modulating Mitochondrial Activities.Journal of proteome research · 2025Article
- Spermidine prevents iron overload-induced impaired bone mass by activating SIRT1/SOD2 signaling in senile rat model.Redox report : communications in free radical research · 2025Article
- The Role and Research Progress of Mitochondria in Sensorineural Hearing Loss.Molecular neurobiology · 2025Review
- Identification and validation of a 9-RBPs-related gene signature associated with prognosis and immune infiltration in bladder cancer based on bioinformatics analysis and machine learning.Translational andrology and urology · 2025Article
- Increased mitophagy protects cochlear hair cells from aminoglycoside-induced damage.Autophagy · 2023Article
- Pathogenic mtDNA variants, in particular single large-scale mtDNA deletions, are strongly associated with post-lingual onset sensorineural hearing loss in primary mitochondrial disease.Molecular genetics and metabolism · 2022Article
- Induced Pluripotent Stem Cells, a Stepping Stone to In Vitro Human Models of Hearing Loss.Cells · 2022Review
- Alternative splicing event associated with immunological features in bladder cancer.Frontiers in oncology · 2022Article
- FGF22 deletion causes hidden hearing loss by affecting the function of inner hair cell ribbon synapses.Frontiers in molecular neuroscience · 2022Article
- Nrf2 Knockout Affected the Ferroptosis Signaling Pathway against Cisplatin-Induced Hair Cell-Like HEI-OC1 Cell Death.Oxidative medicine and cellular longevity · 2022Article
- FOXG1 promotes aging inner ear hair cell survival through activation of the autophagy pathway.Autophagy · 2021Article
- [Progress in genetic susceptibility to aminoglycoside-induced deafness].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2021Review
- Autophagy impairment as a key feature for acetaminophen-induced ototoxicity.Cell death & disease · 2021Article
- Dose-Dependent Pattern of Cochlear Synaptic Degeneration in C57BL/6J Mice Induced by Repeated Noise Exposure.Neural plasticity · 2021Article
- Molecular Behavior of HMGB1 in the Cochlea Following Noise Exposure andFrontiers in cell and developmental biology · 2021Article
- Article
- Deletion of Clusterin Protects Cochlear Hair Cells against Hair Cell Aging and Ototoxicity.Neural plasticity · 2021Article
- Key Signaling Pathways Regulate the Development and Survival of Auditory Hair Cells.Neural plasticity · 2021Review
- Atrial Natriuretic Peptide Promotes Neurite Outgrowth and Survival of Cochlear Spiral Ganglion NeuronsFrontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aminoglycosides are ototoxic to the cochlear hair cells, and mitochondrial dysfunction is one of the major mechanisms behind ototoxic drug-induced hair cell death. TRMU (tRNA 5-methylaminomethyl-2-thiouridylate methyltransferase) is a mitochondrial protein that participates in mitochondrial tRNA modifications, but the role of TRMU in aminoglycoside-induced ototoxicity remains to be elucidated. In this study, we took advantage of the HEI-OC-1 cell line to investigate the role of TRMU in aminoglycoside-induced cell death. We found that TRMU is expressed in both hair cells and HEI-OC-1 cells, and its expression is significantly decreased after 24 h neomycin treatment. We then downregulated TRMU expression with siRNA and found that cell death and apoptosis were significantly increased after neomycin injury. Furthermore, when we down-regulated TRMU expression, we observed significantly increased mitochondrial dysfunction and increased levels of reactive oxygen species (ROS) after neomycin injury, suggesting that TRMU regulates mitochondrial function and ROS levels. Lastly, the antioxidant N-acetylcysteine rescued the mitochondrial dysfunction and cell apoptosis that was induced by TRMU downregulation, suggesting that ROS accumulation contributed to the increased aminoglycosides sensitivity of HEI-OC-1 cells after TRMU downregulation. This study provides evidence that TRMU might be a new therapeutic target for the prevention of aminoglycoside-induced hair cell death.
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