Structural changes in thestrial blood–labyrinth barrier of aged C57BL/6 mice

Neng, Lingling; Zhang, Jinhui; Ju, Yang; Zhang, Fei; López, Iván; Dong, Ming; Shi, Xiaorui

doi:10.1007/s00441-015-2147-2

Cited by 56 publications

(45 citation statements)

References 75 publications

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“…We recently reported that strial PCs regulate TJ expression between ECs and are essential for intrastrial fluid-blood barrier integrity (Neng et al, 2013a). Strial PCs derived from neonatal day-10~15 mice dramatically promote spouting angiogenesis in an in vitro cell-line-based 3D co-culture, as shown in Figure 6 (Neng et al, 2015). Studies from non-cochlear tissues show that PCs also contribute to BM formation by directly synthesizing type IV collagen, glycosaminoglycan, fibronectin, nidogen-1, perlecan , and laminin (Allt et al, 2001; Fisher, 2009; Shepro et al, 1993), and inhibit the activity of destabilizing matrix metalloproteinases (MMP), such as MMP-2 and MMP-9 (Zozulya et al, 2008).…”

Section: Major Components and Structure Of The Cochlear Intrastriamentioning

confidence: 96%

“…A population of around 1220 to 1300 PCs is found in the intrastrial fluid-blood barrier of the normal adult C57/6J mouse cochlea (Neng et al, 2015), as shown in Figure 2A. Extensively branched strial PCs tightly embrace the abluminal strial capillary wall and embed in the BM (Figure 2B).…”

Section: Major Components and Structure Of The Cochlear Intrastriamentioning

confidence: 99%

“…A certain population of PVM/Ms reside in the intrastrial fluid-blood barrier of the normal adult C57/6J mouse cochlea (Neng et al, 2015). It is generally accepted the PVM/Ms originate from cochlear melanocytes derived from the neural crest which have migrated to the stria vascularis during development (Freyer et al, 2011; Steel et al, 1989; Steel et al, 1992; Wakaoka et al, 2013).…”

Section: Major Components and Structure Of The Cochlear Intrastriamentioning

confidence: 99%

“…Recent experimental results from different laboratories demonstrate the potential link of dysfunction of the intrastrial fluid-blood barrier in different hearing disorders, including noise-induced hearing loss (Shi, 2009; Shi et al, 2003; Zhang et al, 2012), age-related hearing loss (Gratton et al, 1996; Gratton et al, 1997; Neng et al, 2015; Ohlemiller et al, 2009), autoimmune disease (Lin et al, 1997; Ruckenstein et al, 1999), genetic hearing disorders (Cohen-Salmon et al, 2007; Fujimura et al, 2005; Jabba et al, 2006; Kitamura et al, 1994), and inflammatory edema and hydrops (Hirose et al, 2014; Zhang et al, 2015). In addition, the barrier is also the point of entry for certain ototoxic drugs, such as cisplatin and gentamicin, which permeate the cochlea through the blood barrier and damage hearing function (Dai et al, 2008; Laurell et al, 2000; Wang et al, 2009).…”

Section: Intrastrial Fluid-blood Barrier and Hearing Disordersmentioning

confidence: 99%

“…Normal function of the stria vascularis (referred to as the “intrastrial fluid-blood barrier”) is critical for maintaining the ionic gradients and endocochlear potential (EP) required for sensory hair cell transduction (Hibino et al, 2010; Marcus et al, 1983; Quraishi et al, 2008; Salt et al, 1987; Spicer et al, 1996; Wangemann, 2002; Zhang et al, 2012). Dysfunction of the stria, including the intrastrial fluid-blood barrier, is considered to be one of the etiologies in a number of hearing disorders, including autoimmune inner ear disease, noise-induced hearing loss, age-related hearing loss , and genetically linked hearing diseases (Lin et al, 1997; Neng et al, 2015; Shi, 2009; Yang et al, 2011; Zhang et al, 2015). Despite the importance of the intrastrial fluid-blood barrier, the physiology of the barrier is largely unknown.…”

Section: Introductionmentioning

confidence: 99%

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Pathophysiology of the cochlear intrastrial fluid-blood barrier (review)

2016

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The blood-labyrinth barrier (BLB) in the stria vascularis is a highly specialized capillary network that controls exchanges between blood and the intrastitial space in the cochlea. The barrier shields the inner ear from blood-born toxic substances and selectively passes ions, fluids, and nutrients to the cochlea, playing an essential role in the maintenance of cochlear homeostasis. Anatomically, the BLB is comprised of endothelial cells (ECs) in the strial microvasculature, elaborated tight and adherens junctions, pericytes (PCs), basement membrane (BM), and perivascular resident macrophage-like melanocytes (PVM/Ms), which together form a complex “cochlear-vascular unit” in the stria vascularis. Physical interactions between the ECs, PCs, and PVM/Ms, as well as signaling between the cells, is critical for controlling vascular permeability and providing a proper environment for hearing function. Breakdown of normal interactions between components of the BLB is seen in a wide range of pathological conditions, including genetic defects and conditions engendered by inflammation, loud sound trauma, and ageing. In this review, we will discuss prevailing views of the structure and function of the strial cochlear-vascular unit (also referred to as the “intrastrial fluid-blood barrier”). We will also discuss the disrupted homeostasis seen in a variety of hearing disorders. Therapeutic targeting of the strial barrier may offer opportunities for improvement of hearing health and amelioration of auditory disorders.

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Section: Major Components and Structure Of The Cochlear Intrastriamentioning

confidence: 96%

Section: Major Components and Structure Of The Cochlear Intrastriamentioning

confidence: 99%

Section: Major Components and Structure Of The Cochlear Intrastriamentioning

confidence: 99%

Section: Intrastrial Fluid-blood Barrier and Hearing Disordersmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Pathophysiology of the cochlear intrastrial fluid-blood barrier (review)

2016

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Understanding the role of inflammation in sensorineural hearing loss: Current goals and future prospects

Li,

Chen,

Lin

et al. 2023

Brain-X

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Sensorineural hearing loss (SNHL) is a common otologic condition caused by damage to hair cells and spiral ganglion neurons that affects transmission pathways. Most of these cells cannot be regenerated, and there has been no breakthrough in regeneration techniques for inner ear cells. SNHL has a high incidence rate and can cause a variety of clinical symptoms, greatly impacting people's daily lives. With limited clinical treatments, the search for critical targets is urgent. Studies have shown that inflammation is prevalent in the pathogenesis of SNHL and plays a significant role in it. Inflammation is a normal body defense response, and a systemic anti‐inflammatory approach is undesirable. It is crucial for us to identify potential targets of inflammation in SNHL and take measures specifically targeting those targets with minimal systemic impact. This paper firstly describes the role of inflammation in various types of SNHL and then provides an overview of the interactions between inflammation and cochlear immunity, cochlear microcirculation, vascular spasm, and glutamate metabolism and finally comprehensively examines the feasibility of targets in these interactions. This paper is expected to facilitate the development of targeted anti‐inflammation for SNHL and provide strategies and approaches for treating clinical SNHL.

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Macrophages in the cochlea; an immunological link between risk factors and progressive hearing loss

Hough

Verschuur

Cunningham

et al. 2021

Glia

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Macrophages are abundant in the cochlea; however, their role in hearing loss is not well understood. Insults to the cochlea, such as noise or insertion of a cochlear implant, cause an inflammatory response, which includes activation of tissue‐resident macrophages. Activation is characterized by changes in macrophage morphology, mediator expression, and distribution. Evidence from other organs shows activated macrophages can become primed, whereby subsequent insults cause an elevated inflammatory response. Primed macrophages in brain pathologies respond to circulating inflammatory mediators by disproportionate synthesis of inflammatory mediators. This signaling occurs behind an intact blood–brain barrier, similar to the blood‐labyrinth barrier in the cochlea. Local tissue damage can occur as the result of mediator release by activated macrophages. Damage is typically localized; however, if it is to structures with limited ability to repair, such as neurons or hair cells within the cochlea, it is feasible that this contributes to the progressive loss of function seen in hearing loss. We propose that macrophages in the cochlea link risk factors and hearing loss. Injury to the cochlea causes local macrophage activation that typically resolves. However, in susceptible individuals, some macrophages enter a primed state. Once primed, these macrophages can be further activated, as a consequence of circulating inflammatory molecules associated with common co‐morbidities. Hypothetically, this would lead to further cochlear damage and loss of hearing. We review the evidence for the role of tissue‐resident macrophages in the cochlea and propose that cochlear macrophages contribute to the trajectory of hearing loss and warrant further study.

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Structural changes in thestrial blood–labyrinth barrier of aged C57BL/6 mice

Cited by 56 publications

References 75 publications

Pathophysiology of the cochlear intrastrial fluid-blood barrier (review)

Pathophysiology of the cochlear intrastrial fluid-blood barrier (review)

Understanding the role of inflammation in sensorineural hearing loss: Current goals and future prospects

Macrophages in the cochlea; an immunological link between risk factors and progressive hearing loss

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