Chloride Conductance Determining Membrane Potential of Rabbit Articular Chondrocytes

Tsuga, K.; Tohse, Noritsugu; Yamada, Masami; Sugimoto, T.; Yamashita, Toshiharu; Ishii, S.; Yabu, Hideyo

doi:10.1007/s00232-001-0112-3

Cited by 32 publications

(48 citation statements)

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“…This finding is apparently not consistent with the previous report that the resting membrane potential in chondrocytes is mainly determined by Cl − but not K + conductance in rabbit chondrocytes (6). It is notable that ]pip was pCa 6.0 than when pCa 7.0.…”

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confidence: 98%

“…It has been suggested that the membrane potential is mainly determined by Cl − conductance in cultured rabbit articular chondrocytes (6). However, our previous study has shown that K + channels also contribute substantially to the regulation of membrane potential changes by histamine in OUMS-27 cells (7).…”

mentioning

confidence: 99%

“…The information about features of Cl − channels responsible for resting membrane conductance are very limited, while huge conductance of swellingactivated Cl − channels, which are apparently not active in isotonic conditions, has been reported recently (11). The much smaller resting Cl − conductance in normal osmotic environments may be attributable to a large conductance and voltage-gated Cl − channel in rabbit articular chondrocytes (6), in which the addition of 1 mM SITS induced membrane depolarization from resting membrane potential of −42 mV. In contrast, in the present study, NFA induced hyperpolarization of 15 mV from the resting membrane potential of −39 mV in OUMS-27 cells under the same experimental conditions.…”

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confidence: 99%

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Contribution of Chloride Channel Conductance to the Regulation of Resting Membrane Potential in Chondrocytes

et al. 2010

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Abstract. The contribution of Cl− conductance relative to that of K + in the regulation of membrane potential was examined using OUMS-27 cells, a model cell-line of human chondrocytes. Application of 100 μM niflumic acid (NFA) and other anion-channel blockers induced significant membrane hyperpolarization. The NFA-sensitive membrane current under voltage-clamp was predominantly Cl − current. Application of NFA induced small but significant increase in intracellular Ca 2+ concentration ([Ca 2+ ] i ) and markedly enhanced the late component of [Ca 2+ ] i rise induced by 1 μM histamine. In conclusion, Cl − conductance substantially contributes to the regulation of resting membrane potential and [Ca 2+ ] i in OUMS-27 cells.

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Contribution of Chloride Channel Conductance to the Regulation of Resting Membrane Potential in Chondrocytes

et al. 2010

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“…Several reports have shown the existence of different chloride channels in chondrocytes [19,20] as well as a Na…”

Section: Discussionmentioning

confidence: 99%

Effects of diadenosine tetraphosphate on FGF9-induced chloride flux changes in achondroplastic chondrocytes

Huete

Guzmán-Aránguez

Ortín

et al. 2011

Purinergic Signalling

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Achondroplasia, the most common type of dwarfism, is characterized by a mutation in the fibroblast growth factor receptor 3 (FGFR3). Achondroplasia is an orphan pathology with no pharmacological treatment so far. However, the possibility of using the dinucleotide diadenosine tetraphosphate (Ap 4 A) with therapeutic purposes in achondroplasia has been previously suggested. The pathogenesis involves the constitutive activation of FGFR3, resulting in altered biochemical and physiological processes in chondrocytes. Some of these altered processes can be influenced by changes in cell volume and ionic currents. In this study, the action of mutant FGFR3 on chondrocyte size and chloride flux in achondroplastic chondrocytes was investigated as well as the effect of the Ap 4 A on these processes triggered by mutant FGFR3. Stimulation with the fibroblast growth factor 9 (FGF9), the preferred ligand for FGFR3, induced an enlarged achondroplastic chondrocyte size and an increase in the intracellular chloride concentration, suggesting the blockade of chloride efflux. Treatment with the Ap 4 A reversed the morphological changes triggered by FGF9 and restored the chloride efflux. These data provide further evidence for the therapeutic potential of this dinucleotide in achondroplasia treatment.

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“…Biochemical and electrophysiological evidence has been presented to demonstrate the expression of a variety of ion channels and transporters in mammalian articular chondrocytes, including tetrodotoxin-sensitive voltage-gated Na + channels (20), voltage-gated K + channels (20,26,27), stretch-activated (mechanosensitive) K + channels (9), voltage-gated Ca 2+ channels (9), voltage-gated Cl − channels (20,28), and Na (29). In the present experiments, isolated rabbit articular chondrocytes were investigated under conditions designed to minimize Na + currents (a holding potential of −30 mV), Ca 2+ currents (removal of Ca…”

Section: Expression Of Collagen Type I and Type Ii In Rabbit Articulamentioning

confidence: 99%

Swelling-Activated Cl− Current in Isolated Rabbit Articular Chondrocytes: Inhibition by Arachidonic Acid

et al. 2009

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Abstract. Articular chondrocytes play an important role in maintaining the structure and function of the cartilage in synovial joints, which is closely influenced by mechanical or osmotic stress. In the present study, isolated rabbit articular chondrocytes were examined during hyposmotic stress using the whole-cell patch-clamp method. When exposed to hyposmotic external solutions (approximately 5% or 32% decrease in osmolarity), isolated rabbit articular chondrocytes exhibited hyposmotic cell swelling, accompanied by the activation of the swellingactivated Cl − current (I Cl,swell ). I Cl,swell was practically time-independent at potentials negative to +50 mV but exhibited rapid inactivation at more positive potentials. I Cl,swell was potently inhibited by the Cl − channel blockers 5-nitro-2-(3-phenylpropylamino)benzoic acid, glibenclamide, and tamoxifen, but was little affected by pimozide. I Cl,swell was also found to be acutely inhibited by arachidonic acid in a concentration-dependent manner with an IC 50 of 0.81 μM. The maximal effect (approximately 100% block) was obtained with 10 μM arachidonic acid. The arachidonic acid metabolites prostaglandin E 2 , leukotriene B 4 , and leukotriene D 4 had no appreciable effect on I Cl,swell , suggesting that the inhibitory effect of arachidonic acid did not require its metabolism. The present study thus reveals the presence of I Cl,swell in rabbit articular chondrocytes that exhibits high sensitivity to direct inhibition by arachidonic acid.

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Chloride Conductance Determining Membrane Potential of Rabbit Articular Chondrocytes

Cited by 32 publications

References 0 publications

Contribution of Chloride Channel Conductance to the Regulation of Resting Membrane Potential in Chondrocytes

Contribution of Chloride Channel Conductance to the Regulation of Resting Membrane Potential in Chondrocytes

Effects of diadenosine tetraphosphate on FGF9-induced chloride flux changes in achondroplastic chondrocytes

Swelling-Activated Cl− Current in Isolated Rabbit Articular Chondrocytes: Inhibition by Arachidonic Acid

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