ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
Damage-induced activation of ERK1/2 in cochlear supporting cells is a hair cell death-promoting signal that depends on extracellular ATP and calcium.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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Who cites it
76 citing papers in PubMed, 116 citations in OpenAlex.
- Article
- Brimonidine Therapy for Protection From Noise-Induced Hearing Loss.Aging cell · 2026Article
- The aryl hydrocarbon receptor is expressed in non-sensory cells in the cochlea and regulates hair cell survival.Frontiers in molecular neuroscience · 2026Article
- Supporting cells orchestrate noise-induced hearing loss via a Gasdermin D-dependent signaling loop with hair cells.Nature communications · 2025Article
- In vivo spontaneous CaNature communications · 2025Article
- Unveiling the Effect of Age and IgE Level on Alopecia Areata: Insights from Comparative RNAseq Analysis.Clinical, cosmetic and investigational dermatology · 2025Article
- Mechanisms driving the functional maturation of the developing mammalian auditory pathway.Current topics in developmental biology · 2025Review
- Noise induces Ca2+ signaling waves and Chop/S-Xbp1 expression in the hearing cochlea.JCI insight · 2024Article
- Pharmacological Approaches to Hearing Loss.Pharmacological reviews · 2024Review
- Reprogramming withPNAS nexus · 2024Article
- ERK1/2 Inhibition via the Oral Administration of Tizaterkib Alleviates Noise-Induced Hearing Loss While Tempering down the Immune Response.International journal of molecular sciences · 2024Article
- Trametinib, a MEK1/2 Inhibitor, Protects Mice from Cisplatin- and Noise-Induced Hearing Loss.Pharmaceuticals (Basel, Switzerland) · 2024Article
- FDA-Approved MEK1/2 Inhibitor, Trametinib, Protects Mice from Cisplatin and Noise-Induced Hearing Loss.bioRxiv : the preprint server for biology · 2024Article
- Oseltamivir (Tamiflu), a Commonly Prescribed Antiviral Drug, Mitigates Hearing Loss in Mice.bioRxiv : the preprint server for biology · 2024Article
- KSR1 Knockout Mouse Model Demonstrates MAPK Pathway's Key Role in Cisplatin- and Noise-induced Hearing Loss.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Spiral ganglion neuron degeneration in aminoglycoside-deafened rats involves innate and adaptive immune responses not requiring complement.Frontiers in molecular neuroscience · 2024Article
- Damage-evoked signals in cochlear neurons and supporting cells.Frontiers in neurology · 2024Review
- Dabrafenib protects from cisplatin-induced hearing loss in a clinically relevant mouse model.JCI insight · 2023Article
- KSR1 knockout mouse model demonstrates MAPK pathway's key role in cisplatin- and noise-induced hearing loss.bioRxiv : the preprint server for biology · 2023Article
- ERK1/2 Inhibition Alleviates Noise-Induced Hearing Loss While Tempering Down the Immune Response.bioRxiv : the preprint server for biology · 2023Article
16 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Acoustic overstimulation and ototoxic drugs can cause permanent hearing loss as a result of the damage and death of cochlear hair cells. Relatively little is known about the signaling pathways triggered by such trauma, although a significant role has been described for the c-Jun N-terminal kinase [one of the mitogen-activated protein kinases (MAPKs)] pathway. We investigated the role of another MAPK family, the extracellularly regulated kinases 1 and 2 (ERK1/2) during hair cell damage in neonatal cochlear explants. Within minutes of subjecting explants to mechanical damage, ERK1/2 were transiently activated in Deiters' and phalangeal cells but not in hair cells. The activation of ERK1/2 spread along the length of the cochlea, reaching its peak 5-10 min after damage onset. Release of extracellular ATP and the presence of functional connexin proteins were critical for the activation and spread of ERK1/2. Damage elicited an intercellular Ca(2+) wave in the hair cell region in the first seconds after damage. In the absence of Ca(2+) influx, the intercellular Ca(2+) wave and the magnitude and spread of ERK1/2 activation were reduced. Treatment with the aminoglycoside neomycin produced a similar pattern of ERK1/2 activation in supporting cells surrounding pyknotic hair cells. When ERK1/2 activation was prevented, there was a reduction in the number of pyknotic hair cells. Thus, activation of ERK1/2 in cochlear supporting cells in vitro is a common damage signaling mechanism that acts to promote hair cell death, indicating a direct role for supporting cells in regulating hair cell death.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.