ArticlePloS one2012
Overactivation of Notch1 signaling induces ectopic hair cells in the mouse inner ear in an age-dependent manner.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 44 citations in OpenAlex.
- Integrated scRNAseq analyses of mouse cochlear supporting cells reveal the involvement of Ezh2 in hair cell regeneration.Molecular biology reports · 2024Article
- Gata3 is required in late proneurosensory development for proper sensory cell formation and organization.Scientific reports · 2023Article
- Gata3 is Required in Late Proneurosensory Development for Proper Sensory Cell Formation and Organization.Research square · 2023Article
- Stem Cell-Based Therapies in Hearing Loss.Frontiers in cell and developmental biology · 2021Review
- Research Progress of Hair Cell Protection Mechanism.Neural plasticity · 2020Review
- Age-related transcriptome changes in Sox2+ supporting cells in the mouse cochlea.Stem cell research & therapy · 2019Article
- Increased levels of miR-124 in human dental pulp stem cells alter the expression of neural markers.Journal of otology · 2019Article
- Unidirectional and stage-dependent roles of Notch1 in Wnt-responsive Lgr5Frontiers of medicine · 2019Article
- Regeneration of Cochlear Hair Cells and Hearing Recovery through Hes1 Modulation with siRNA Nanoparticles in Adult Guinea Pigs.Molecular therapy : the journal of the American Society of Gene Therapy · 2018Article
- Spontaneous Hair Cell Regeneration Is Prevented by Increased Notch Signaling in Supporting Cells.Frontiers in cellular neuroscience · 2018Article
- Shaping of inner ear sensory organs through antagonistic interactions between Notch signalling and Lmx1a.eLife · 2017Article
- Role of Wnt and Notch signaling in regulating hair cell regeneration in the cochlea.Frontiers of medicine · 2016Review
- Canonical Notch signaling plays an instructive role in auditory supporting cell development.Scientific reports · 2016Article
- Mammalian Cochlear Hair Cell Regeneration and Ribbon Synapse Reformation.Neural plasticity · 2016Review
- Sensory hair cell development and regeneration: similarities and differences.Development (Cambridge, England) · 2015Review
- Development of hair cells in inner ear is associated with expression and promoter methylation of Notch-1 in postnatal mice.International journal of clinical and experimental medicine · 2015Article
- Changes in the regulation of the Notch signaling pathway are temporally correlated with regenerative failure in the mouse cochlea.Frontiers in cellular neuroscience · 2015Article
- Auditory hair cell-specific deletion of p27Kip1 in postnatal mice promotes cell-autonomous generation of new hair cells and normal hearing.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Signaling mechanisms controlling cranial placode neurogenesis and delamination.Developmental biology · 2014Review
- Activated notch causes deafness by promoting a supporting cell phenotype in developing auditory hair cells.PloS one · 2014Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundDuring mouse inner ear development, Notch1 signaling first specifies sensory progenitors, and subsequently controls progenitors to further differentiate into either hair cells (HCs) or supporting cells (SCs). Overactivation of NICD (Notch1 intracellular domain) at early embryonic stages leads to ectopic HC formation. However, it remains unclear whether such an effect can be elicited at later embryonic or postnatal stages, which has important implications in mouse HC regeneration by reactivation of Notch1 signaling. METHODOLOGY/PRINCIPAL
findingsWe performed comprehensive in vivo inducible overactivation of NICD at various developmental stages. In CAG(CreER+); Rosa26-NICD(loxp/+) mice, tamoxifen treatment at embryonic day 10.5 (E10.5) generated ectopic HCs in the non-sensory regions in both utricle and cochlea, whereas ectopic HCs only appeared in the utricle when tamoxifen was given at E13. When tamoxifen was injected at postnatal day 0 (P0) and P1, no ectopic HCs were observed in either utricle or cochlea. Interestingly, Notch1 signaling induced new HCs in a non-cell-autonomous manner, because the new HCs did not express NICD. Adjacent to the new HCs were cells expressing the SC marker Sox10 (either NICD+ or NICD-negative). CONCLUSIONS/SIGNIFICANCE: Our data demonstrate that the developmental stage determines responsiveness of embryonic otic precursors and neonatal non-sensory epithelial cells to NICD overactivation, and that Notch 1 signaling in the wild type, postnatal inner ear is not sufficient for generating new HCs. Thus, our genetic mouse model is suitable to test additional pathways that could synergistically interact with Notch1 pathway to produce HCs at postnatal ages.
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