Vitamin D upregulates expression of ECaC1 mRNA in semicircular canal

Yamauchi, Daisuke; Raveendran, Nithya N.; Pondugula, Satyanarayana R.; Kampalli, Suresh B; Sanneman, Joel D.; Harbidge, Donald G.; Marcus, Daniel C.

doi:10.1016/j.bbrc.2005.04.053

Cited by 59 publications

(52 citation statements)

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“…Previously, we reported the expression of the epithelial Ca 2+ channels TRPV5 and TRPV6 in primary cultures of SCCD epithelial cells (44). Because of the known sensitivity of the TRPV5/6 channels to external pH (46), we hypothesized that low pH of vestibular endolymph due to absence of the Cl -/ exchanger pendrin inhibits TRPV5 and TRPV6, and consequently leads to higher [Ca 2+ ] in endolymph.…”

Section: Discussionmentioning

confidence: 96%

“…Primary cultures of Wistar rat SCCD were prepared and incubated in DMEM/F-12 (Invitrogen, #12500-062) supplemented with 5% fetal bovine serum, penicillin (100 U/ml), streptomycin (100 μg/ml) as described previously (44). Primary cultures of SCCD cells from rat were used to study transport function since murine SCCD cells have been observed to not proliferate in culture.…”

Section: Cellular Uptake Measurementsmentioning

confidence: 99%

“…We tested whether Ca 2+ absorption is stimulated by exposure to vitamin D since transcript expression of two genes involved in epithelial Ca 2+ absorption, TRPV5 and calbindin, is upregulated (44). Stimulation of transport would therefore serve as part of the fingerprint for the involvement of this Ca 2+ transport system in vestibular function.…”

Section: Increased Ca 2+ Absorption By 125(oh) 2 Dmentioning

confidence: 99%

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Lack of pendrin HCO₃⁻transport elevates vestibular endolymphatic [Ca²⁺] by inhibition of acid-sensitive TRPV5 and TRPV6 channels

Nakaya¹,

Harbidge²,

Wangemann³

et al. 2007

American Journal of Physiology-Renal Physiology

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The low Ca 2+ concentration of mammalian endolymph in the inner ear is required for normal hearing and balance. We reported [Yamauchi et al. Biochem Biophys Res Commun, 2005] that the epithelial Ca 2+ channels TRPV5 and TRPV6 are expressed in the vestibular system and that TRPV5 expression is stimulated by 1,25-dihydroxyvitamin D 3 (1,25(OH) 2 D 3 ), as also reported in kidney. TRPV5/6 channels are known to be inhibited by extracellular acidic pH. Endolymphatic pH, [Ca 2+ ] and transepithelial potential of the utricle (UP) were measured in Cl -/ exchanger pendrin (SLC26A4) knockout mice in vivo. Slc26a4 -/-mice exhibit reduced pH and UP and increased [Ca 2+ ]. Monolayers of primary cultures of rat semicircular canal duct (SCCD) cells were grown on permeable supports and cellular uptake of 45 Ca 2+ was measured individually from the apical and basolateral sides. Net uptake of 45 Ca 2+ was greater after incubation with 1,25(OH) 2 D 3 . Net 45 Ca 2+ absorption was dramatically inhibited by low apical pH and was stimulated by apical alkaline pH. Gadolinium, lanthanum and ruthenium red reduced apical uptake. These observations support the notion that one aspect of vestibular dysfunction in Pendred syndrome is a pathological elevation of endolymphatic [Ca 2+ ] due to luminal acidification and consequent inhibition of TRPV5/6-mediated Ca 2+ absorption.

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Section: Discussionmentioning

confidence: 96%

Section: Cellular Uptake Measurementsmentioning

confidence: 99%

Section: Increased Ca 2+ Absorption By 125(oh) 2 Dmentioning

confidence: 99%

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Lack of pendrin HCO₃⁻transport elevates vestibular endolymphatic [Ca²⁺] by inhibition of acid-sensitive TRPV5 and TRPV6 channels

Nakaya¹,

Harbidge²,

Wangemann³

et al. 2007

American Journal of Physiology-Renal Physiology

Self Cite

121

116

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“…They contain more than 90% calcite (crystalized calcium carbonate), and they are the only calcite-based biological structures acting in physiological processes in human beings, whereas other two systems, bone and teeth, contain calcium phosphate [12,13] . Calcium and carbonate levels in the endolymph are critical for normal otoconial function, which is primarily provided by a calcium channel transport system expressed in the inner ear [14] . When the ultrastructural dysmorphology of human otoconia was investigated by Walther et al [15] , they found that otoconia may have various degrees of degeneration, from minor to major changes.…”

Section: Discussionmentioning

confidence: 99%

The Role of Oxidative Stress and Inflammatory Mediators in Benign Paroxysmal Positional Vertigo

Gucluturk

Unal²,

İsmi³

et al. 2016

Int Adv Otol

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OBJECTIVE:Benign paroxysmal positional vertigo (BPPV) is the most common peripheral cause of vertigo. It can be defined as transient vertigo induced by rapid changes in head position associated with a characteristic paroxysmal positional nystagmus. The aim of this study was to search for the possible role of oxidative stress and inflammatory mediators in the pathogenesis of BPPV. MATERIALS and METHODS:Total antioxidant status as well as paraoxonase, tumor necrosis factor alpha, interleukin (IL) 6, and IL-1β levels were evaluated in peripheral venous serum samples of 30 BPPV and 30 control patients. RESULTS:Total antioxidant status levels were lower in the BPPV group than in the control group (p=0.008). After Epley's repositioning maneuver in the vertigo group, there was a statistically significant decline in IL-1β levels at the first and third month visits (p=0.014 for first month and p=0.013 for third month). CONCLUSION:Our findings suggested that IL-1β and oxidative stress contributed to the pathogenesis of BPPV.

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“…The otoconia are in a dynamic state, and calcium and potassium are required to mineralize otoconia and to maintain any turnover in the otolith [26 ,27] . Two mechanisms have been proposed to explain the relationship between BPPV and abnormal calcium metabolism: 1) a disturbed internal structure of the otoconia or their interconnections and attachment to the gelatinous matrix and 2) a reduced capacity to dissolve the dislodged otoconia owing to increased concentration of free calcium in the endolymph, resulting from increased calcium resorption [28,29] .To this extent, both the cochlea and labyrinth were found to express crucial genes needed to constitute a Ca 2+ absorption mechanism to maintain low levels of endolymphatic Ca 2+ in order to sustain normal hearing and balance functions [30] . The Ca 2+ absorptive system comprises an apical membrane entry pathway (TRPV5 and TRPV6 channels), a cytosolic Ca 2+ buffer protein (calbindin-D9K and calbindin-D28K), and basolateral Ca 2+ exit pathways (sodium-calcium exchangers -NCX-) and plasma membrane Ca 2+ -ATPases (PMCA) [31] .…”

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confidence: 99%

A Pilot Study Using Intratympanic Methylprednisolone for Treatment of Persistent Posterior Canal Benign Paroxysmal Positional Vertigo

Pérez¹,

Franco²,

Oliva³

et al. 2016

Int Adv Otol

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OBJECTIVE:To assess the effect of intratympanic methylprednisolone (ITMP) in posterior canal benign paroxysmal positional vertigo (BPPV) that fails treatment involving repositioning maneuver in a case series. MATERIALS and METHODS:Nine patients with persistent posterior canal BPPV after 6 or more repositioning maneuvers were treated by ITMP (two weekly doses of 0.3-0.4 mL at 40 mg/mL) before repeating the repositioning procedures. RESULTS:Following ITMP treatment, 7 out of 9 patients were relieved of their symptoms and did not exhibit positional nystagmus after 1 or 2 repositioning maneuvers. The number of positional maneuvers performed before and after ITMP treatment in these 7 patients showed a statistically significant (p=0.016) reduction in the amount of repositioning treatments required. None of the 7 respondent patients showed any relapses during the follow-up period (follow-up range: 11-95 months). CONCLUSION:Administering ITMP before resuming repositioning procedures can be a useful treatment for persistent BPPV of the posterior canal. Intratympanic (IT) steroids are often used to treat inner ear disorders such as sudden idiopathic sensorineural hearing loss, autoimmune hearing loss, and Ménière's disease [14] . Corticosteroids exert their effects in the inner ear after interacting with intracellular glucocorticoid receptors by producing metabolic and anti-inflammatory effects. It is also known that glucocorticoid receptors are widespread throughout the inner ear, including semicircular canal duct epithelial cells, where they facilitate cation absorption via sodium channels [15][16][17] . KEYWORDS:Thus, considering the possibility of an inflammatory process of the labyrinth or an imbalance of Na + and Ca 2+ in the endolymph could be related with the intractability of BPPV, we have carried out a pilot study to assess the effect of IT methylprednisolone (ITMP) in persistent posterior canal BPPV. MATERIALS and METHODSThis prospective study included patients from 3 different hospitals. From January 2006 to March 2014, we diagnosed 187 patients affected from unilateral posterior canal BPPV. None of them had any symptoms or signs of central nervous system (CNS) disease. A complete otoneurological examination, including otoscopy, audiometry, head thrust test, spontaneous nystagmus recording, gaze-evoked nystagmus test, cover test, and Romberg and Fukuda tests, were performed in all the cases.The diagnosis of posterior canal BPPV was made by Dix-Hallpike test, showing a mixed vertical and torsional nystagmus beating toward the undermost ear, with appropriate latency and duration, and the direction of the nystagmus reversed on resuming the upright position. In every patient, the roll test and head hyperextension test were also performed in order to rule out lateral or superior canal BPPV.Patients with BPPV were treated by Epley or Semont maneuvers. We carried out only one of those maneuvers in every session. Each session, weekly programmed, began with a Dix-Hallpike test; if it was positive for the same posterior...

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Vitamin D upregulates expression of ECaC1 mRNA in semicircular canal

Cited by 59 publications

References 13 publications

Lack of pendrin HCO₃⁻transport elevates vestibular endolymphatic [Ca²⁺] by inhibition of acid-sensitive TRPV5 and TRPV6 channels

Lack of pendrin HCO₃⁻transport elevates vestibular endolymphatic [Ca²⁺] by inhibition of acid-sensitive TRPV5 and TRPV6 channels

The Role of Oxidative Stress and Inflammatory Mediators in Benign Paroxysmal Positional Vertigo

A Pilot Study Using Intratympanic Methylprednisolone for Treatment of Persistent Posterior Canal Benign Paroxysmal Positional Vertigo

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Vitamin D upregulates expression of ECaC1 mRNA in semicircular canal

Cited by 59 publications

References 13 publications

Lack of pendrin HCO3−transport elevates vestibular endolymphatic [Ca2+] by inhibition of acid-sensitive TRPV5 and TRPV6 channels

Lack of pendrin HCO3−transport elevates vestibular endolymphatic [Ca2+] by inhibition of acid-sensitive TRPV5 and TRPV6 channels

The Role of Oxidative Stress and Inflammatory Mediators in Benign Paroxysmal Positional Vertigo

A Pilot Study Using Intratympanic Methylprednisolone for Treatment of Persistent Posterior Canal Benign Paroxysmal Positional Vertigo

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Lack of pendrin HCO₃⁻transport elevates vestibular endolymphatic [Ca²⁺] by inhibition of acid-sensitive TRPV5 and TRPV6 channels

Lack of pendrin HCO₃⁻transport elevates vestibular endolymphatic [Ca²⁺] by inhibition of acid-sensitive TRPV5 and TRPV6 channels