Spontaneous recovery of cochlear fibrocytes after severe degeneration caused by acute energy failure

Mizutari, Kunio

doi:10.3389/fphar.2014.00198

Cited by 7 publications

(9 citation statements)

References 33 publications

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“…Immunohistochemistry revealed that these cells were SLFs and the examination at different time points revealed that the number of those cells declined as the mice aged. Since slow-cycling cells in general contain a stem/progenitor cell population, manipulating those fibrocytes may accelerate repopulation, leading to the development of promising therapeutic strategies for treating some types of sensorineural hearing loss, such as presbyacusis [ 25 ].…”

Section: Discussionmentioning

confidence: 99%

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

Watanabe

Fujioka

et al. 2017

PLoS ONE

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Cochlear spiral ligament fibrocytes (SLFs) play essential roles in the physiology of hearing including ion recycling and the generation of endocochlear potential. In adult animals, SLFs can repopulate after damages, yet little is known about the characteristics of proliferating cells that support SLFs’ self-renewal. Here we report in detail about the characteristics of cycling cells in the spiral ligament (SL). Fifteen P6 mice and six noise-exposed P28 mice were injected with 5-bromo-2′-deoxyuridine (BrdU) for 7 days and we chased BrdU retaining cells for as long as 60 days. Immunohistochemistry revealed that the BrdU positive IB4 (an endotherial marker) negative cells expressed an early SLF marker Pou3f4 but negative for cleaved-Caspase 3. Marker studies revealed that type 3 SLFs displayed significantly higher percentage of BrdU+ cells compared to other subtypes. Notably, the cells retained BrdU until P72, demonstrating they were dividing slowly.In the noise-damaged mice, in contrast to the loss of the other types, the number of type 3 SLFs did not altered and the BrdU incorporating- phosphorylated Histone H3 positive type 3 cells were increased from day 1 to 14 after noise exposure. Furthermore, the cells repopulating type 1 area, where the cells diminished profoundly after damage, were positive for the type 3 SLF markers. Collectively, in the latral wall of the cochlea, type 3 SLFs have the stem cell capacity and may contribute to the endogenous regeneration of lateral wall spiral ligament. Manipulating type 3 cells may be employed for potential regenerative therapies.

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Section: Discussionmentioning

confidence: 99%

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

Watanabe

Fujioka

et al. 2017

PLoS ONE

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“…The majority of SSNHL cases still remain idiopathic. 7,49 Several hypotheses about the pathophysiology of idiopathic SSNHL have already been proposed; 50–63 the most widely accepted theories are direct vascular damage, 40–50 cochlear membrane rupture, 51,52 auto-immunity or immune-mediated disorder, 52–57 viral infection, 4,58–63 and stress response theory. 59 However, at least in some cases, an etiologic agent (either vascular, infective, or immune-mediated) could damage hair cells, indirectly, disrupting their metabolic activity, reversibly or irreversibly.…”

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

“…the stria vasularis or spiral ligament fibrocytes) and consequentially causing sudden loss of hearing (partial or total); or (2) the possibility of hearing recovery (partial or total) due to the spontaneous recuperation of the endocochlear ionic environment. 29,[60][61][62] Also, an alteration of inner-ear vascular permeability could explain a sudden hearing defect: an endothelial dysfunction of the microcirculation of the inner ear, for example due to oxidative stress, 64 may cause a disruption of the normal ionic exchanges between blood and the stria vascularis and between the stria vascularis and the perilymph. 56 Furthermore, the lateral wall of the cochlea participates in the regulation of inner ear pH and, as a consequence, a sudden damage of the stria vascularis and/or spiral ligament could lead to a cochlear pH alteration.…”

Section: Pathophysiology Of Ssnhl and Inner-ear Electrolytic Disordersmentioning

confidence: 99%

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Sudden sensorineural hearing loss: Is there a connection with inner ear electrolytic disorders? A literature review

Ciorba

Corazzi

Bianchini

et al. 2016

Int J Immunopathol Pharmacol

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Electrolytic disorders of the inner ear represent a model that could be implicated in partially explaining the pathogenesis of sudden sensorineural hearing loss (SSNHL). Different types of electrolytes and different inner-ear loci are involved in cochlear homeostasis physiologically, to ensure the maintenance of an ion-balanced cochlear environment allowing a normal hair cell function. It has been hypothesized that a sudden loss of endocochlear potential, due to a rapid disruption of the inner ear fluid osmolality, could be responsible for a deterioration of the hearing function caused by damaged hair cells. The aim of this paper was to review the current literature and identify sources which might validate/fortify the hypothesis that inner ear electrolytic disorders have a role in the etiopathogenesis of SSNHL. The data in the literature underline the importance of ionic homeostasis in the inner ear, but they do not support a direct link between SSNHL and electrolyte disorders/imbalances. There is marginal evidence from otoacoustic emissions research that an indirect link might be present.

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“…Secondly, after trauma has occurred, there is often inflammation and influx of macrophages to the injured region. Several studies have demonstrated that the spiral ligament contains bone marrow-derived cells that can differentiate into macrophages (89). Macrophages are known to promote regeneration after injury (90).…”

Section: Recovery Of the Spiral Ligament After Traumamentioning

confidence: 99%

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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Spontaneous recovery of cochlear fibrocytes after severe degeneration caused by acute energy failure

Cited by 7 publications

References 33 publications

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

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

Sudden sensorineural hearing loss: Is there a connection with inner ear electrolytic disorders? A literature review

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

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