ArticleScientific reports2017
c-Myb knockdown increases the neomycin-induced damage to hair-cell-like HEI-OC1 cells in vitro.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 61 citations in OpenAlex.
- Effects ofNutrients · 2024Article
- Early-Onset Hearing Loss in Mouse Models of Alzheimer's Disease and Increased DNA Damage in the Cochlea.Aging biology · 2024Article
- Increased mitophagy protects cochlear hair cells from aminoglycoside-induced damage.Autophagy · 2023Article
- Cisplatin ototoxicity mechanism and antagonistic intervention strategy: a scope review.Frontiers in cellular neuroscience · 2023Review
- Elucidation of the mechanism of miR-122-5p in mediating FOXO3 injury and apoptosis of mouse cochlear hair cells induced by hydrogen peroxide.Experimental and therapeutic medicine · 2022Article
- c-Myb protects cochlear hair cells from cisplatin-induced damage via the PI3K/Akt signaling pathway.Cell death discovery · 2022Article
- Novel m.4268T>C mutation in the mitochondrial tRNAWorld journal of clinical cases · 2022Article
- FGF22 deletion causes hidden hearing loss by affecting the function of inner hair cell ribbon synapses.Frontiers in molecular neuroscience · 2022Article
- Puerarin alleviates the ototoxicity of gentamicin by inhibiting the mitochondria‑dependent apoptosis pathway.Molecular medicine reports · 2021Article
- Prevention of acquired sensorineural hearing loss in mice by in vivo Htra2 gene editing.Genome biology · 2021Article
- Autophagy impairment as a key feature for acetaminophen-induced ototoxicity.Cell death & disease · 2021Article
- Noise-Induced Hearing Loss: Updates on Molecular Targets and Potential Interventions.Neural plasticity · 2021Review
- 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
- Dose-Dependent Pattern of Cochlear Synaptic Degeneration in C57BL/6J Mice Induced by Repeated Noise Exposure.Neural plasticity · 2021Article
- Atrial Natriuretic Peptide Promotes Neurite Outgrowth and Survival of Cochlear Spiral Ganglion NeuronsFrontiers in cell and developmental biology · 2021Article
- Autophagy: A Novel Horizon for Hair Cell Protection.Neural plasticity · 2021Review
- Hair Cell Protection from Ototoxic Drugs.Neural plasticity · 2021Review
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
c-Myb is a transcription factor that plays a key role in cell proliferation, differentiation, and apoptosis. It has been reported that c-Myb is expressed within the chicken otic placode, but whether c-Myb exists in the mammalian cochlea, and how it exerts its effects, has not been explored yet. Here, we investigated the expression of c-Myb in the postnatal mouse cochlea and HEI-OC1 cells and found that c-Myb was expressed in the hair cells (HCs) of mouse cochlea as well as in cultured HEI-OC1 cells. Next, we demonstrated that c-Myb expression was decreased in response to neomycin treatment in both cochlear HCs and HEI-OC1 cells, suggesting an otoprotective role for c-Myb. We then knocked down c-Myb expression with shRNA transfection in HEI-OC1 cells and found that c-Myb knockdown decreased cell viability, increased expression of pro-apoptotic factors, and enhanced cell apoptosis after neomycin insult. Mechanistic studies revealed that c-Myb knockdown increased cellular levels of reactive oxygen species and decreased Bcl-2 expression, both of which are likely to be responsible for the increased sensitivity of c-Myb knockdown cells to neomycin. This study provides evidence that c-Myb might serve as a new target for the prevention of aminoglycoside-induced HC loss.
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