Effect of Urea on Osmolality of Perilymph

Juhn, Steven K.; Prado, Sergio; Rybak, Leonard P.

doi:10.1001/archotol.1979.00790210036008

Cited by 26 publications

(5 citation statements)

References 20 publications

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“…Osmolality for the randomly selected tumour secretions did not significantly deviate from control media, being 323, 316 and 324 mOsm/kg for control media, VS7 and VS8 secretions, respectively. The values were near the expected value of 335 mOsm/kg in perilymph for mammals 19 .…”

Section: Resultssupporting

confidence: 50%

Secreted Factors from Human Vestibular Schwannomas Can Cause Cochlear Damage

Dilwali

Landegger

Soares

et al. 2015

Sci Rep

110

120

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Vestibular schwannomas (VSs) are the most common tumours of the cerebellopontine angle. Ninety-five percent of people with VS present with sensorineural hearing loss (SNHL); the mechanism of this SNHL is currently unknown. To establish the first model to study the role of VS-secreted factors in causing SNHL, murine cochlear explant cultures were treated with human tumour secretions from thirteen different unilateral, sporadic VSs of subjects demonstrating varied degrees of ipsilateral SNHL. The extent of cochlear explant damage due to secretion application roughly correlated with the subjects’ degree of SNHL. Secretions from tumours associated with most substantial SNHL resulted in most significant hair cell loss and neuronal fibre disorganization. Secretions from VSs associated with good hearing or from healthy human nerves led to either no effect or solely fibre disorganization. Our results are the first to demonstrate that secreted factors from VSs can lead to cochlear damage. Further, we identified tumour necrosis factor alpha (TNFα) as an ototoxic molecule and fibroblast growth factor 2 (FGF2) as an otoprotective molecule in VS secretions. Antibody-mediated TNFα neutralization in VS secretions partially prevented hair cell loss due to the secretions. Taken together, we have identified a new mechanism responsible for SNHL due to VSs.

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Section: Resultssupporting

confidence: 50%

Secreted Factors from Human Vestibular Schwannomas Can Cause Cochlear Damage

Dilwali

Landegger

Soares

et al. 2015

Sci Rep

110

120

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“…Urea tests have long been used to aid the diagnosis of vestibular and hearing impairment in patients with Ménière's disease (Babin and Bumsted, 1980; Imoto and Stahle, 1983) and urea has also been used to temporarily improve hearing in these patients (Angelborg et al, 1977). This effect was thought to be partially due to the changes in perilymph osmolality caused by urea (Juhn et al, 1979). Interestingly, the urea cycle was altered in multiple brain regions in neurodegenerative diseases such as Huntington's disease (Patassini et al, 2015) and Alzheimer's disease (Xu et al, 2016), which suggests that brain urea metabolism may play an important role in maintaining neuronal function.…”

Section: Discussionmentioning

confidence: 99%

Brain Metabolic Changes in Rats following Acoustic Trauma

Zhu

et al. 2017

Front. Neurosci.

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Acoustic trauma is the most common cause of hearing loss and tinnitus in humans. However, the impact of acoustic trauma on system biology is not fully understood. It has been increasingly recognized that tinnitus caused by acoustic trauma is unlikely to be generated by a single pathological source, but rather a complex network of changes involving not only the auditory system but also systems related to memory, emotion and stress. One obvious and significant gap in tinnitus research is a lack of biomarkers that reflect the consequences of this interactive “tinnitus-causing” network. In this study, we made the first attempt to analyse brain metabolic changes in rats following acoustic trauma using metabolomics, as a pilot study prior to directly linking metabolic changes to tinnitus. Metabolites in 12 different brain regions collected from either sham or acoustic trauma animals were profiled using a gas chromatography mass spectrometry (GC/MS)-based metabolomics platform. After deconvolution of mass spectra and identification of the molecules, the metabolomic data were processed using multivariate statistical analysis. Principal component analysis showed that metabolic patterns varied among different brain regions; however, brain regions with similar functions had a similar metabolite composition. Acoustic trauma did not change the metabolite clusters in these regions. When analyzed within each brain region using the orthogonal projection to latent structures discriminant analysis sub-model, 17 molecules showed distinct separation between control and acoustic trauma groups in the auditory cortex, inferior colliculus, superior colliculus, vestibular nucleus complex (VNC), and cerebellum. Further metabolic pathway impact analysis and the enrichment overview with network analysis suggested the primary involvement of amino acid metabolism, including the alanine, aspartate and glutamate metabolic pathways, the arginine and proline metabolic pathways and the purine metabolic pathway. Our results provide the first metabolomics evidence that acoustic trauma can induce changes in multiple metabolic pathways. This pilot study also suggests that the metabolomic approach has the potential to identify acoustic trauma-specific metabolic shifts in future studies where metabolic changes are correlated with the animal's tinnitus status.

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“…The contents of urea and glycerol are commonly used for diagnosis of Meniere’s disease. Urea can increase the permeability gradient between blood and inner ear fluid and reduce the volume of endolymph hydrops [7, 30, 87]. The steady state of the volume, pressure, and chemical composition in the endolymph is crucial for the electromechanical conduction of sound in the ear.…”

Section: Ut-b Proteinsmentioning

confidence: 99%

Physiological functions of urea transporter B

Liu

et al. 2019

Pflugers Arch - Eur J Physiol

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Urea transporters (UTs) are membrane proteins in the urea transporter protein A (UT-A) and urea transporter protein B (UT-B) families. UT-B is mainly expressed in endothelial cell membrane of the renal medulla and in other tissues, including the brain, heart, pancreas, colon, bladder, bone marrow, and cochlea. UT-B is responsible for the maintenance of urea concentration, male reproductive function, blood pressure, bone metabolism, and brain astrocyte and cardiac functions. Its deficiency and dysfunction contribute to the pathogenesis of many diseases. Actually, UT-B deficiency increases the sensitivity of bladder epithelial cells to apoptosis triggers in mice and UT-B-null mice develop II-III atrioventricular block and depression. The expression of UT-B in the rumen of cow and sheep may participate in digestive function. However, there is no systemic review to discuss the UT-B functions. Here, we update research approaches to understanding the functions of UT-B.

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Effect of Urea on Osmolality of Perilymph

Cited by 26 publications

References 20 publications

Secreted Factors from Human Vestibular Schwannomas Can Cause Cochlear Damage

Secreted Factors from Human Vestibular Schwannomas Can Cause Cochlear Damage

Brain Metabolic Changes in Rats following Acoustic Trauma

Physiological functions of urea transporter B

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