ArticleCell death & disease2015
Bmi1 regulates auditory hair cell survival by maintaining redox balance.
Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 57 citations in OpenAlex.
- Kolliker's Organ and Its Functional Role in the Development of Corti's Organ and Auditory Systems.Audiology research · 2025Review
- Retinal BMI1 Expression Preserves Photoreceptors in Sodium-Iodate-Induced Oxidative Stress Models.International journal of molecular sciences · 2025Article
- Conditional Overexpression of Neuritin in Supporting Cell Protects Cochlear Hair Cell and Delays Age-Related Hearing Loss by Enhancing Autophagy.International journal of molecular sciences · 2025Article
- From genomic discovery to application in age-related hearing loss: a global bibliometric and cross-ethnic analysis.Frontiers in aging neuroscience · 2025Article
- Direct targeting of mitochondria by cisplatin leads to cytotoxicity in zebrafish lateral-line hair cells.iScience · 2024Article
- BRCA1 Promotes Repair of DNA Damage in Cochlear Hair Cells and Prevents Hearing Loss.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- BMI1 is required for melanocyte stem cell maintenance and hair pigmentation.Pigment cell & melanoma research · 2023Article
- Article
- In vivo investigation of mitochondria in lateral line afferent neurons and hair cells.Hearing research · 2023Review
- Unfolded protein response inhibits KAT2B/MLKL-mediated necroptosis of hepatocytes by promoting BMI1 level to ubiquitinate KAT2B.Open medicine (Warsaw, Poland) · 2023Article
- Chronic neurotransmission increases the susceptibility of lateral-line hair cells to ototoxic insults.eLife · 2022Article
- The Spatiotemporal Expression of Ring1B in the Postnatal Mouse Cochlea.The journal of international advanced otology · 2022Article
- Dync1li1 is required for the survival of mammalian cochlear hair cells by regulating the transportation of autophagosomes.PLoS genetics · 2022Article
- The Vascular Niche for Adult Cardiac Progenitor Cells.Antioxidants (Basel, Switzerland) · 2022Review
- Sox2 overexpression alleviates noise-induced hearing loss by inhibiting inflammation-related hair cell apoptosis.Journal of neuroinflammation · 2022Article
- Epigenetic Alterations under Oxidative Stress in Stem Cells.Oxidative medicine and cellular longevity · 2022Review
- Kölliker's organ-supporting cells and cochlear auditory development.Frontiers in molecular neuroscience · 2022Review
- Article
- Characterization ofFrontiers in genetics · 2021Article
- Knockdown of Foxg1 in supporting cells increases the trans-differentiation of supporting cells into hair cells in the neonatal mouse cochlea.Cellular and molecular life sciences : CMLS · 2020Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species (ROS) accumulation are involved in noise- and ototoxic drug-induced hair cell loss, which is the major cause of hearing loss. Bmi1 is a member of the Polycomb protein family and has been reported to regulate mitochondrial function and ROS level in thymocytes and neurons. In this study, we reported the expression of Bmi1 in mouse cochlea and investigated the role of Bmi1 in hair cell survival. Bmi1 expressed in hair cells and supporting cells in mouse cochlea. Bmi1(-/-) mice displayed severe hearing loss and patched outer hair cell loss from postnatal day 22. Ototoxic drug-induced hair cells loss dramatically increased in Bmi1(-/-) mice compared with that in wild-type controls both in vivo and in vitro, indicating Bmi1(-/-) hair cells were significantly more sensitive to ototoxic drug-induced damage. Cleaved caspase-3 and TUNEL staining demonstrated that apoptosis was involved in the increased hair cell loss of Bmi1(-/-) mice. Aminophenyl fluorescein and MitoSOX Red staining showed the level of free radicals and mitochondrial ROS increased in Bmi1(-/-) hair cells due to the aggravated disequilibrium of antioxidant-prooxidant balance. Furthermore, the antioxidant N-acetylcysteine rescued Bmi1(-/-) hair cells from neomycin injury both in vitro and in vivo, suggesting that ROS accumulation was mainly responsible for the increased aminoglycosides sensitivity in Bmi1(-/-) hair cells. Our findings demonstrate that Bmi1 has an important role in hair cell survival by controlling redox balance and ROS level, thus suggesting that Bmi1 may work as a new therapeutic target for the prevention of hair cell death.
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