ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Cisplatin ototoxicity blocks sensory regeneration in the avian inner ear.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 44 citations in OpenAlex.
- Development of the inner ear and regeneration of hair cells after hearing impairment.Fundamental research · 2025Review
- Cisplatin vestibulotoxicity: a current review.Frontiers in surgery · 2024Review
- Loxhd1b inhibits the hair cell development in zebrafish: Possible relation to the BDNF/TrkB/ERK pathway.Frontiers in cellular neuroscience · 2022Article
- Supporting Cells and Their Potential Roles in Cisplatin-Induced Ototoxicity.Frontiers in neuroscience · 2022Review
- Mechanosensory neuron regeneration in adultDevelopment (Cambridge, England) · 2021Article
- Dynamic patterns of YAP1 expression and cellular localization in the developing and injured utricle.Scientific reports · 2021Article
- Up-regulation of autophagy and apoptosis of cochlear hair cells in mouse models for deafness.Archives of medical science : AMS · 2021Article
- Cisplatin-induced hair cell loss in zebrafish neuromasts is accompanied by protein nitration and Lmo4 degradation.Toxicology and applied pharmacology · 2021Article
- Aminoglycoside- and Cisplatin-Induced Ototoxicity: Mechanisms and Otoprotective Strategies.Cold Spring Harbor perspectives in medicine · 2019Review
- Musashi-1 is the candidate of the regulator of hair cell progenitors during inner ear regeneration.BMC neuroscience · 2017Article
- Emodin mitigates the oxidative stress induced by cisplatin in osteosarcoma MG63 cells.Oncology letters · 2016Article
- Live imaging the phagocytic activity of inner ear supporting cells in response to hair cell death.Cell death and differentiation · 2015Article
- Transient alteration of the vestibular calyceal junction and synapse in response to chronic ototoxic insult in rats.Disease models & mechanisms · 2015Article
- An integrated view of cisplatin-induced nephrotoxicity and ototoxicity.Toxicology letters · 2015Review
- Spontaneous regeneration of cochlear supporting cells after neonatal ablation ensures hearing in the adult mouse.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Cisplatin exposure damages resident stem cells of the mammalian inner ear.Developmental dynamics : an official publication of the American Association of Anatomists · 2014Article
- Apaf-1 inhibitors protect from unwanted cell death in in vivo models of kidney ischemia and chemotherapy induced ototoxicity.PloS one · 2014Article
- Inner ear supporting cells: rethinking the silent majority.Seminars in cell & developmental biology · 2013Review
- Changes in the adult vertebrate auditory sensory epithelium after trauma.Hearing research · 2013Review
- A brief history of hair cell regeneration research and speculations on the future.Hearing research · 2013Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cisplatin is a chemotherapeutic agent that is widely used in the treatment of solid tumors. Ototoxicity is a common side effect of cisplatin therapy and often leads to permanent hearing loss. The sensory organs of the avian ear are able to regenerate hair cells after aminoglycoside ototoxicity. This regenerative response is mediated by supporting cells, which serve as precursors to replacement hair cells. Given the antimitotic properties of cisplatin, we examined whether the avian ear was also capable of regeneration after cisplatin ototoxicity. Using cell and organ cultures of the chick cochlea and utricle, we found that cisplatin treatment caused apoptosis of both auditory and vestibular hair cells. Hair cell death in the cochlea occurred in a unique pattern, progressing from the low-frequency (distal) region toward the high-frequency (proximal) region. We also found that cisplatin caused a dose-dependent reduction in the proliferation of cultured supporting cells as well as increased apoptosis in those cells. As a result, we observed no recovery of hair cells after ototoxic injury caused by cisplatin. Finally, we explored the potential for nonmitotic hair cell recovery via activation of Notch pathway signaling. Treatment with the gamma-secretase inhibitor N-[N-(3,5-difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester failed to promote the direct transdifferentiation of supporting cells into hair cells in cisplatin-treated utricles. Taken together, our data show that cisplatin treatment causes maintained changes to inner ear supporting cells and severely impairs the ability of the avian ear to regenerate either via proliferation or by direct transdifferentiation.
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