ArticleCell death & disease2015
XBP1 mitigates aminoglycoside-induced endoplasmic reticulum stress and neuronal cell death.
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 50 papers.
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Who cites it
50 citing papers in PubMed, 77 citations in OpenAlex.
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- Blocking acid-sensing ion channel 1a attenuates bilirubin-induced ototoxicity in cochlear organotypic culture.Fundamental research · 2026Article
- Translational error in mice increases with ageing in an organ-dependent manner.Nature communications · 2025Article
- Mutations in unfolded protein response regulator ATF6 cause hearing and vision loss syndrome.The Journal of clinical investigation · 2025Article
- GRP78 protein metabolism in obese and diabetic rats: a study of its role in metabolic disorders.Diabetology & metabolic syndrome · 2024Article
- Insights into the molecular underlying mechanisms and therapeutic potential of endoplasmic reticulum stress in sensorineural hearing loss.Frontiers in molecular neuroscience · 2024Review
- Bile Acid Application in Cell-Targeting for Molecular Receptors in Relation to Hearing: A Comprehensive Review.Current drug targets · 2024Review
- Otoprotection against aminoglycoside- and cisplatin-induced ototoxicity focusing on the upstream drug uptake pathway.Journal of the Chinese Medical Association : JCMA · 2024Review
- TMTC4 is a hair cell-specific human deafness gene.JCI insight · 2023Article
- Mechanisms and Impact of Aminoglycoside-Induced Vestibular Deficits.American journal of audiology · 2023Review
- Macrophage depletion attenuates degeneration of spiral ganglion neurons in kanamycin-induced unilateral hearing loss model.Scientific reports · 2023Article
- Aminoglycosides-Related Ototoxicity: Mechanisms, Risk Factors, and Prevention in Pediatric Patients.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Endoplasmic Reticulum Stress and Autophagy Are Involved in Hepatotoxicity Induced by Tributyltin.Toxics · 2023Article
- TMEM30A is essential for hair cell polarity maintenance in postnatal mouse cochlea.Cellular & molecular biology letters · 2023Article
- Article
- The Genomics of Auditory Function and Disease.Annual review of genomics and human genetics · 2022Review
- Efficacy of controlled-flux electrolyzed acidic solution in dogs with otitis externa.Veterinary research forum : an international quarterly journal · 2022Article
- Premature aging in mice with error-prone protein synthesis.Science advances · 2022Article
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10 authors at 3 institutions in 2 countries.
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Abstract
Here we study links between aminoglycoside-induced mistranslation, protein misfolding and neuropathy. We demonstrate that aminoglycosides induce misreading in mammalian cells and assess endoplasmic reticulum (ER) stress and unfolded protein response (UPR) pathways. Genome-wide transcriptome and proteome analyses revealed upregulation of genes related to protein folding and degradation. Quantitative PCR confirmed induction of UPR markers including C/EBP homologous protein, glucose-regulated protein 94, binding immunoglobulin protein and X-box binding protein-1 (XBP1) mRNA splicing, which is crucial for UPR activation. We studied the effect of a compromised UPR on aminoglycoside ototoxicity in haploinsufficient XBP1 (XBP1(+/-)) mice. Intra-tympanic aminoglycoside treatment caused high-frequency hearing loss in XBP1(+/-) mice but not in wild-type littermates. Densities of spiral ganglion cells and synaptic ribbons were decreased in gentamicin-treated XBP1(+/-) mice, while sensory cells were preserved. Co-injection of the chemical chaperone tauroursodeoxycholic acid attenuated hearing loss. These results suggest that aminoglycoside-induced ER stress and cell death in spiral ganglion neurons is mitigated by XBP1, masking aminoglycoside neurotoxicity at the organismal level.
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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.