Characterization of slow-cycling cells in the mouse cochlear lateral wall

Li, Yang; Watanabe, Kotaro; Fujioka, Masato; Ogawa, Kaoru

doi:10.1371/journal.pone.0179293

Cited by 13 publications

(13 citation statements)

References 32 publications

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“…Interestingly, examination of P16 DTX-treated and control cochleae revealed that edema of the stria vascularis was no longer present and endothelial cells surrounding LW blood vessels were comparable to those present in control cochleae (Figures 9N–O’ ). Our analysis of macrophage-depleted cochleae agrees with recent studies that reported recovery/self-repairing capability of the cochlear LW following damage (Mizutari et al, 2011 ; Stevens et al, 2014 ; Li et al, 2017 ).…”

Section: Resultssupporting

confidence: 91%

Macrophage-Mediated Glial Cell Elimination in the Postnatal Mouse Cochlea

Brown

Xing

Noble

et al. 2017

Front. Mol. Neurosci.

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Hearing relies on the transmission of auditory information from sensory hair cells (HCs) to the brain through the auditory nerve. This relay of information requires HCs to be innervated by spiral ganglion neurons (SGNs) in an exclusive manner and SGNs to be ensheathed by myelinating and non-myelinating glial cells. In the developing auditory nerve, mistargeted SGN axons are retracted or pruned and excessive cells are cleared in a process referred to as nerve refinement. Whether auditory glial cells are eliminated during auditory nerve refinement is unknown. Using early postnatal mice of either sex, we show that glial cell numbers decrease after the first postnatal week, corresponding temporally with nerve refinement in the developing auditory nerve. Additionally, expression of immune-related genes was upregulated and macrophage numbers increase in a manner coinciding with the reduction of glial cell numbers. Transient depletion of macrophages during early auditory nerve development, using transgenic CD11bDTR/EGFP mice, resulted in the appearance of excessive glial cells. Macrophage depletion caused abnormalities in myelin formation and transient edema of the stria vascularis. Macrophage-depleted mice also showed auditory function impairment that partially recovered in adulthood. These findings demonstrate that macrophages contribute to the regulation of glial cell number during postnatal development of the cochlea and that glial cells play a critical role in hearing onset and auditory nerve maturation.

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Section: Resultssupporting

confidence: 91%

Macrophage-Mediated Glial Cell Elimination in the Postnatal Mouse Cochlea

Brown

Xing

Noble

et al. 2017

Front. Mol. Neurosci.

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“…Functional hearing recovery is strongly associated with morphological remodeling of the cochlear lateral wall and repair of the SLFs [24,25]. There is increasing evidence that SLFs have a remarkably low threshold for noise-induced loss, which may explain the prevalence of missing fibrocytes in humans [26].…”

Section: Introductionmentioning

confidence: 99%

Acoustic Trauma Modulates Cochlear Blood Flow and Vasoactive Factors in a Rodent Model of Noise-Induced Hearing Loss

Shin

Lyu

Jeong

et al. 2019

IJMS

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Noise exposure affects the organ of Corti and the lateral wall of the cochlea, including the stria vascularis and spiral ligament. Although the inner ear vasculature and spiral ligament fibrocytes in the lateral wall consist of a significant proportion of cells in the cochlea, relatively little is known regarding their functional significance. In this study, 6-week-old male C57BL/6 mice were exposed to noise trauma to induce transient hearing threshold shift (TTS) or permanent hearing threshold shift (PTS). Compared to mice with TTS, mice with PTS exhibited lower cochlear blood flow and lower vessel diameter in the stria vascularis, accompanied by reduced expression levels of genes involved in vasodilation and increased expression levels of genes related to vasoconstriction. Ultrastructural analyses by transmission electron microscopy revealed that the stria vascularis and spiral ligament fibrocytes were more damaged by PTS than by TTS. Moreover, mice with PTS expressed significantly higher levels of proinflammatory cytokines in the cochlea (e.g., IL-1β, IL-6, and TNF-α). Overall, our findings suggest that cochlear microcirculation and lateral wall pathologies are differentially modulated by the severity of acoustic trauma and are associated with changes in vasoactive factors and inflammatory responses in the cochlea.

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“…Therefore, type III SLFs could play a potential role in regenerative therapies. However, more research is needed to confirm this hypothesis (76).…”

Section: Histopathology Of the Spiral Limbus And Lateral Wallmentioning

confidence: 98%

On the Role of Fibrocytes and the Extracellular Matrix in the Physiology and Pathophysiology of the Spiral Ligament

et al. 2020

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The spiral ligament in the cochlea has been suggested to play a significant role in the pathophysiology of different etiologies of strial hearing loss. Spiral ligament fibrocytes (SLFs), the main cell type in the lateral wall, are crucial in maintaining the endocochlear potential and regulating blood flow. SLF dysfunction can therefore cause cochlear dysfunction and thus hearing impairment. Recent studies have highlighted the role of SLFs in the immune response of the cochlea. In contrast to sensory cells in the inner ear, SLFs (more specifically type III fibrocytes) have also demonstrated the ability to regenerate after different types of trauma such as drug toxicity and noise. SLFs are responsible for producing proteins, such as collagen and cochlin, that create an adequate extracellular matrix to thrive in. Any dysfunction of SLFs or structural changes to the extracellular matrix can significantly impact hearing function. However, SLFs may prove useful in restoring hearing by their potential to regenerate cells in the spiral ligament.

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Characterization of slow-cycling cells in the mouse cochlear lateral wall

Cited by 13 publications

References 32 publications

Macrophage-Mediated Glial Cell Elimination in the Postnatal Mouse Cochlea

Macrophage-Mediated Glial Cell Elimination in the Postnatal Mouse Cochlea

Acoustic Trauma Modulates Cochlear Blood Flow and Vasoactive Factors in a Rodent Model of Noise-Induced Hearing Loss

On the Role of Fibrocytes and the Extracellular Matrix in the Physiology and Pathophysiology of the Spiral Ligament

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