ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
Cisplatin-induced hair cell death requires STAT1 and is attenuated by epigallocatechin gallate.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
54 citing papers in PubMed, 92 citations in OpenAlex.
- Phase II trial of post-operative radiotherapy with concurrent cisplatin plus panitumumab in patients with high-risk, resected head and neck cancer.Annals of oncology : official journal of the European Society for Medical Oncology · 2016Trial
- Article
- From Ototoxicity to Otoprotection: Mechanism and Protective Strategies in Cisplatin Therapy.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Early downregulation of hair cell (HC)-specific genes in the vestibular sensory epithelium during chronic ototoxicity.Journal of biomedical science · 2025Article
- Studies on the mechanism of ototoxic action of cisplatin and the antagonistic effect of polyphenolic compounds.Frontiers in pharmacology · 2025Review
- Cisplatin-Induced Hearing Loss, Oxidative Stress, and Antioxidants as a Therapeutic Strategy-A State-of-the-Art Review.Antioxidants (Basel, Switzerland) · 2024Review
- Rutin Attenuates Gentamycin-induced Hair Cell Injury in the Zebrafish Lateral Line via Suppressing STAT1.Molecular neurobiology · 2024Article
- Novel Synergistic Approach for Bioactive Macromolecules: Evaluating the Efficacy of Goat Placenta Extract in PEGylated Liposomes and Microspicules for Chemotherapy-Induced Hair Loss.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Unveiling the Role of Oxidative Stress in Cochlear Hair Cell Death: Prospective Phytochemical Therapeutics against Sensorineural Hearing Loss.International journal of molecular sciences · 2024Review
- What is the Reason That the Pharmacological Future of Chemotherapeutics in the Treatment of Lung Cancer Could Be Most Closely Related to Nanostructures? Platinum Drugs in Therapy of Non-Small and Small Cell Lung Cancer and Their Unexpected, Possible Interactions. The Review.International journal of nanomedicine · 2024Review
- Exploring causal associations of antioxidants from supplements and diet with attention deficit/hyperactivity disorder in European populations: a Mendelian randomization analysis.Frontiers in nutrition · 2024Article
- Apelin-13 protects against cisplatin-induced ototoxicity by inhibiting apoptosis and regulating STAT1 and STAT3.Archives of toxicology · 2023Article
- Pro-Inflammatory Signalling PRRopels Cisplatin-Induced Toxicity.International journal of molecular sciences · 2022Review
- Oxidative Stress and Inflammation Caused by Cisplatin Ototoxicity.Antioxidants (Basel, Switzerland) · 2021Review
- Lmo4 Deficiency Enhances Susceptibility to Cisplatin-Induced Cochlear Apoptosis and Hearing Loss.Molecular neurobiology · 2021Article
- Auditory function analysis in immunodeficient STAT1 knock-out mice: Considerations for viral infection models.Neuroscience letters · 2021Article
- Preferential Cochleotoxicity of Cisplatin.Frontiers in neuroscience · 2021Review
- Hair Cell Protection from Ototoxic Drugs.Neural plasticity · 2021Review
- Autophagy: A Novel Horizon for Hair Cell Protection.Neural plasticity · 2021Review
- Up-regulation of autophagy and apoptosis of cochlear hair cells in mouse models for deafness.Archives of medical science : AMS · 2021Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Cisplatin is a chemotherapy drug that frequently causes auditory impairment due to the death of mechanosensory hair cells. Cisplatin ototoxicity may result from oxidative stress, DNA damage, and inflammatory cytokines. The transcription factor STAT1, an important mediator of cell death, can regulate all of these processes in other cell types. We used cultured utricles from mature Swiss Webster mice to investigate the role of STAT1 in cisplatin-induced hair cell death. We show that STAT1 phosphorylation is an early event in both hair cells and support cells after exposure of utricles to cisplatin. STAT1 phosphorylation peaked after 4 h of cisplatin exposure and returned to control levels by 8 h of exposure. The STAT1 inhibitor epigallocatechin gallate (EGCG) attenuated STAT1 phosphorylation in cisplatin-treated utricles and resulted in concentration-dependent increases in hair cell survival at 24 h postexposure. Furthermore, we show that utricular hair cells from STAT1-deficient mice are resistant to cisplatin toxicity. EGCG failed to provide additional protection from cisplatin in STAT1-deficient mice, further supporting the hypothesis that the protective effects of EGCG are due to its inhibition of STAT1. Treatment with IFN-gamma, which also causes STAT1 activation, also induced hair cell death in wild-type but not STAT1-deficient mice. These results show that STAT1 is required for maximal cisplatin-induced hair cell death in the mouse utricle and suggest that treatment with EGCG may be a useful strategy for prevention of cisplatin ototoxicity.
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What OpenQuestion holds
Registered trials
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.