ArticleFrontiers in cellular neuroscience2015
Macrophage recruitment and epithelial repair following hair cell injury in the mouse utricle.
Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 49 citations in OpenAlex.
- The Enigmatic Presence of Actin Rings, Actin Cables and Ectopic Hair Cells in the Vestibular Maculae of Mice and Humans.Journal of the Association for Research in Otolaryngology : JARO · 2026Article
- Injury-Induced Remodeling of Junctional Actin Bands in the Vestibular Maculae of Mice and Chicks: Implications for Sensory Regeneration.Journal of the Association for Research in Otolaryngology : JARO · 2026Article
- Sentinels or saboteurs, the Janus face of cochlear-resident macrophages in hearing loss: spatiotemporal distribution, pathophysiological functions, and translational potential.Journal of neuroinflammation · 2025Review
- Injury-Induced Remodeling of Junctional Actin Bands in the Vestibular Maculae of Mice and Chicks: Implications for Sensory Regeneration.bioRxiv : the preprint server for biology · 2025Article
- Genetic polymorphisms in human CXJournal of neuroinflammation · 2025Article
- AAV-mediated inner ear gene delivery triggers mild host immune responses in the mammalian inner ear.Molecular therapy. Methods & clinical development · 2025Article
- Crosstalk Signaling Between the Epithelial and Non-Epithelial Compartments of the Mouse Inner Ear.Journal of the Association for Research in Otolaryngology : JARO · 2025Article
- Early control of cochlear viral load limits cochlear inflammation and prevents virus-induced sensorineural hearing loss.Journal of neuroinflammation · 2025Article
- Trophic and temporal dynamics of macrophage biology in human inner ear organogenesis.Frontiers in immunology · 2025Article
- Article
- Immuno-surveillance and protection of the human cochlea.Frontiers in neurology · 2024Article
- The Stria Vascularis in Mice and Humans Is an Early Site of Age-Related Cochlear Degeneration, Macrophage Dysfunction, and Inflammation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Macrophage-related immune responses in inner ear: a potential therapeutic target for sensorineural hearing loss.Frontiers in neuroscience · 2023Review
- Chronic suppurative otitis media causes macrophage-associated sensorineural hearing loss.Journal of neuroinflammation · 2022Article
- ASK1 is a novel molecular target for preventing aminoglycoside-induced hair cell death.Journal of molecular medicine (Berlin, Germany) · 2022Article
- Semi-automated quantification of hair cells in the mature mouse utricle.Hearing research · 2022Article
- The Time Course of Monocytes Infiltration After Acoustic Overstimulation.Frontiers in cellular neuroscience · 2022Article
- Distribution of Immune Cells Including Macrophages in the Human Cochlea.Frontiers in neurology · 2021Review
- Programmed Cell Death Recruits Macrophages Into the Developing Mouse Cochlea.Frontiers in cell and developmental biology · 2021Article
- Relationships between Intrascalar Tissue, Neuron Survival, and Cochlear Implant Function.Journal of the Association for Research in Otolaryngology : JARO · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The sensory organs of the inner ear possess resident populations of macrophages, but the function of those cells is poorly understood. In many tissues, macrophages participate in the removal of cellular debris after injury and can also promote tissue repair. The present study examined injury-evoked macrophage activity in the mouse utricle. Experiments used transgenic mice in which the gene for the human diphtheria toxin receptor (huDTR) was inserted under regulation of the Pou4f3 promoter. Hair cells in such mice can be selectively lesioned by systemic treatment with diphtheria toxin (DT). In order to visualize macrophages, Pou4f3-huDTR mice were crossed with a second transgenic line, in which one or both copies of the gene for the fractalkine receptor CX3CR1 were replaced with a gene for GFP. Such mice expressed GFP in all macrophages, and mice that were CX3CR1(GFP/GFP) lacked the necessary receptor for fractalkine signaling. Treatment with DT resulted in the death of ∼70% of utricular hair cells within 7 days, which was accompanied by increased numbers of macrophages within the utricular sensory epithelium. Many of these macrophages appeared to be actively engulfing hair cell debris, indicating that macrophages participate in the process of 'corpse removal' in the mammalian vestibular organs. However, we observed no apparent differences in injury-evoked macrophage numbers in the utricles of CX3CR1(+/GFP) mice vs. CX3CR1(GFP/GFP) mice, suggesting that fractalkine signaling is not necessary for macrophage recruitment in these sensory organs. Finally, we found that repair of sensory epithelia at short times after DT-induced hair cell lesions was mediated by relatively thin cables of F-actin. After 56 days recovery, however, all cell-cell junctions were characterized by very thick actin cables.
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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.