ArticleMolecular neurobiology2019
Downregulated UCHL1 Accelerates Gentamicin-Induced Auditory Cell Death via Autophagy.
Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 16 citations in OpenAlex.
- The ubiquitin-proteasome system and proteostasis in the cochlea and sensorineural hearing disorders.Molecular biomedicine · 2026Review
- Targeting Autophagy for Otoprotection: Translating Basic Mechanisms into Clinical Strategies.International journal of molecular sciences · 2026Review
- Morphological analysis of autophagy in axonal degeneration in gracile axonal dystrophy mice.Experimental animals · 2025Article
- Article
- Abnormal Cholesterol Metabolism and Lysosomal Dysfunction Induce Age-Related Hearing Loss by Inhibiting mTORC1-TFEB-Dependent Autophagy.International journal of molecular sciences · 2023Article
- The cochlea is built to last a lifetime.Hearing research · 2023Review
- UCHL1 regulated by Sp1 ameliorates cochlear hair cell senescence and oxidative damage.Experimental and therapeutic medicine · 2023Article
- Cellular autophagy, the compelling roles in hearing function and dysfunction.Frontiers in cellular neuroscience · 2022Review
- Bioinformatic Analysis of the Perilymph Proteome to Generate a Human Protein Atlas.Frontiers in cell and developmental biology · 2022Article
- Article
- Parkin, an E3 Ubiquitin Ligase, Plays an Essential Role in Mitochondrial Quality Control in Parkinson's Disease.Cellular and molecular neurobiology · 2021Review
- Deubiquitinases: Modulators of Different Types of Regulated Cell Death.International journal of molecular sciences · 2021Review
- Autophagy: A Novel Horizon for Hair Cell Protection.Neural plasticity · 2021Review
- Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The clinical use of aminoglycoside antibiotics is partly limited by their ototoxicity. The pathogenesis of aminoglycoside-induced ototoxicity still remains unknown. Here, RNA-sequencing was conducted to identify differentially expressed genes in rat cochlear organotypic cultures treated with gentamicin (GM), and 232 and 43 genes were commonly up- and downregulated, respectively, at day 1 and 2 after exposure. Ubiquitin carboxyl-terminal hydrolase isozyme L1 (Uchl1) was one of the downregulated genes whose expression was prominent in spiral ganglion cells (SGCs), lateral walls, as well as efferent nerve terminal and nerve fibers. We further investigated if a deficit of Uchl1 in organotypic cochlea and the House Ear Institute-Organ of Corti 1 (HEI-OC1) cells accelerates ototoxicity. We found that a deficit in Uchl1 accelerated GM-induced ototoxicity by showing a decreased number of SGCs and nerve fibers in organotypic cochlear cultures and HEI-OC1 cells. Furthermore, Uchl1-depleted HEI-OC1 cells revealed an increased number of autophagosomes accompanied by decreased lysosomal fusion. These data indicate that the downregulation of Uchl1 following GM treatment is deleterious to auditory cell survival, which results from the impaired autophagic flux. Our results provide evidence that UCHL1-dependent autophagic flux may have a potential as an otoprotective target for the treatment of GM-induced auditory cell death.
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Registered trials
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