ArticlePloS one2013
Conditional deletion of pten leads to defects in nerve innervation and neuronal survival in inner ear development.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 15 citations in OpenAlex.
- The mTOR Pathway in Hearing Disorders: Mechanistic Links to Aging, Regeneration, and Neurodegeneration.Molecular neurobiology · 2026Review
- mTOR Signaling: New Insights into Cancer, Cardiovascular Diseases, Diabetes and Aging.International journal of molecular sciences · 2023Article
- Activation of Rictor/mTORC2 signaling acts as a pivotal strategy to protect against sensorineural hearing loss.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- PRDX1 activates autophagy via the PTEN-AKT signaling pathway to protect against cisplatin-induced spiral ganglion neuron damage.Autophagy · 2021Article
- mTOR Signaling in the Inner Ear as Potential Target to Treat Hearing Loss.International journal of molecular sciences · 2021Review
- Tuberous sclerosis complex-mediated mTORC1 overactivation promotes age-related hearing loss.The Journal of clinical investigation · 2018Article
- Autophagy in the Vertebrate Inner Ear.Frontiers in cell and developmental biology · 2017Review
- Activation of PI3K signaling prevents aminoglycoside-induced hair cell death in the murine cochlea.Biology open · 2016Article
- Gene expression profiling of the inner ear.Journal of anatomy · 2016Review
- Patterns of gene expression associated with Pten deficiency in the developing inner ear.PloS one · 2014Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
All cellular phenomena and developmental events, including inner ear development, are modulated through harmonized signaling networks. Phosphatase and tensin homolog deleted on chromosome 10 (PTEN), a tumor suppressor, is a major signaling component involved in cross talk with key regulators of development; i.e., Wnt, Notch, and bone morphogenetic proteins. Although Pten function has been studied in various systems, its role in inner ear development is poorly understood. Here, we used inner ear-specific Pten conditional knockout mice and examined the characteristics of the inner ear. In a detailed analysis of the phenotype, reduced cochlear turning and widened epithelia were observed. Phalloidin staining of sensory epithelium revealed that hair cell patterns were disturbed; i.e., additional rows of hair cells were discovered. The neural abnormality revealed a reduction in and disorganization of nerve fibers, including apoptosis at the neural precursor stage. Pten deficiency induced increased phosphorylation of Akt at Ser473. The elevation of inhibitory glycogen synthase kinase 3β Ser9 phosphorylation (pGSK3β) was sustained until the neuronal differentiation stage at embryonic day 14.5, instead of pGSK3β downregulation. This is the first report on the influence of Pten/Akt/GSK3β signaling on the development of spiral ganglia. These results suggest that Pten is required for the maintenance of neuroblast number, neural precursors, and differentiation in the inner ear.
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