Expression of CLCN Voltage-gated Chloride Channel Genes in Human Blood Vessels

Lamb, Fred S.; Clayton, Gerald H.; Liu, Bei-Xing; Smith, Roderic L.; Barna, Thomas J.; Schutte, Brian C.

doi:10.1006/jmcc.1998.0901

Cited by 49 publications

(34 citation statements)

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“…Addition of .Ϫ through an anion channel. ClC-3 is the most abundant chloride channel in endothelial cells (Lamb et al, 1999) and knockout of this channel results in compensatory changes in cell membrane protein expression and function (Yamamoto-Mizuma et al, 2004). Selective knockdown of ClC-3 using siRNA resulted in a significant reduction in the HE transient similar to that observed by anion channel inhibition with DIDS.…”

Section: Superoxide Flux-mediated Ros Generationmentioning

confidence: 94%

“…This result provides evidence that mitochondrial ROS generation occurs as a result of intracellular Ca 2ϩ mobilization (Madesh et al, 2005) .Ϫ flux across the plasma membrane. Because ClC-3 is the most abundant anion channel in endothelial cells (Lamb et al, 1999) and is inhibitable by DIDS (Hirotsu et al, 1999), we chose to assess whether knockdown of ClC-3 elicits a reduction in HE fluorescence similar to that demonstrated by DIDS. Electroporation efficiently delivered siRNA to MPMVECs as evidenced by microscopic evaluation of Cy3-labeled GAPDH siRNA ( Figure 6A).…”

Section: Receptor-mediated Increase In He Fluorescencementioning

confidence: 99%

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Superoxide Flux in Endothelial Cells via the Chloride Channel-3 Mediates Intracellular Signaling

Hawkins

Madesh

Kirkpatrick

et al. 2007

MBoC

169

150

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.؊ resulted in rapid and concentration-dependent transient HE oxidation that was followed by a progressive and nonreversible increase in nuclear HE fluorescence. These fluorescence changes were inhibited by superoxide dismutase (SOD), the anion channel blocker DIDS, and selective silencing of the chloride channel-3 (ClC-3) by treatment with siRNA. Extracellular O 2 .؊ triggered Ca 2؉ release in turn triggered mitochondrial membrane potential alterations that were followed by mitochondrial O 2 .؊ production and cellular apoptosis. These "signaling" effects of O 2 .؊ were prevented by DIDS treatment, by depletion of intracellular Ca 2؉ stores with thapsigargin and by chelation of intracellular Ca 2؉ . This study demonstrates that O 2 .؊ flux across the endothelial cell plasma membrane occurs through ClC-3 channels and induces intracellular Ca 2؉ release, which activates mitochondrial O 2 .؊ generation.

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Section: Superoxide Flux-mediated Ros Generationmentioning

confidence: 94%

Section: Receptor-mediated Increase In He Fluorescencementioning

confidence: 99%

Superoxide Flux in Endothelial Cells via the Chloride Channel-3 Mediates Intracellular Signaling

Hawkins

Madesh

Kirkpatrick

et al. 2007

MBoC

169

150

View full text Add to dashboard Cite

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“…In rats, ClC-5 is expressed in other tissues besides the kidney, such as brain, lungs, liver, endothelial cells, and colon (31)(32)(33)36). In addition, the human ClC-5 channel is also expressed in endothelial cells, suggesting that the distribution of ClC-5 may not be restricted to the kidney (37).…”

Section: Clc-5 Chloride Channel and Protein Endocytosismentioning

confidence: 99%

“…The hypothesis that higher levels of urinary calcium lead to precipitation of calcium salts and then to stone formation is well accepted today (1,2,8,9). Although ClC-5 seems to be expressed mainly in the human kidney (the major site of the disease), it is also expressed in rat colon, brain, and lungs (33,34,(36)(37)(38)48,49) and in Xenopus oocytes (50).…”

Section: The Role Of Clc-5 In Mineral Metabolismmentioning

confidence: 99%

“…The distribution of ClC-5 mRNA along the rat nephron reveals that this chloride channel is more abundant in the S 3 segments of proximal tubules, in the cortical and medullary thick ascending limb of Henles loop, and in cortical collecting ducts (CCD) (33,34,36,37). An independent group using in situ hybridization further confirmed the expression of the ClC-5 channel on these segments (32).…”

Section: The Role Of Clc-5 In Mineral Metabolismmentioning

confidence: 99%

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ClC-5 chloride channel and kidney stones: what is the link?

Silva

Morales

Lopes

2001

Braz J Med Biol Res

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Nephrolithiasis is one of the most common diseases in the Western world. The disease manifests itself with intensive pain, sporadic infections, and, sometimes, renal failure. The symptoms are due to the appearance of urinary stones (calculi) which are formed mainly by calcium salts. These calcium salts precipitate in the renal papillae and/ or within the collecting ducts. Inherited forms of nephrolithiasis related to chromosome X (X-linked hypercalciuric nephrolithiasis or XLN) have been recently described. Hypercalciuria, nephrocalcinosis, and male predominance are the major characteristics of these diseases. The gene responsible for the XLN forms of kidney stones was cloned and characterized as a chloride channel called ClC-5. The ClC-5 chloride channel belongs to a superfamily of voltage-gated chloride channels, whose physiological roles are not completely understood. The objective of the present review is to identify recent advances in the molecular pathology of nephrolithiasis, with emphasis on XLN. We also try to establish a link between a chloride channel like ClC-5, hypercalciuria, failure in urine acidification and protein endocytosis, which could explain the symptoms exhibited by XLN patients.

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Endothelial and Smooth Muscle Cell Ion Channels in Pulmonary Vasoconstriction and Vascular Remodeling

Makino

Firth

Yuan

2011

Comprehensive Physiology

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The pulmonary circulation is a low resistance and low pressure system. Sustained pulmonary vasoconstriction and excessive vascular remodeling often occur under pathophysiological conditions such as in patients with pulmonary hypertension. Pulmonary vasoconstriction is a consequence of smooth muscle contraction. Many factors released from the endothelium contribute to regulating pulmonary vascular tone, while the extracellular matrix in the adventitia is the major determinant of vascular wall compliance. Pulmonary vascular remodeling is characterized by adventitial and medial hypertrophy due to fibroblast and smooth muscle cell proliferation, neointimal proliferation, intimal, and plexiform lesions that obliterate the lumen, muscularization of precapillary arterioles, and in situ thrombosis. A rise in cytosolic free Ca2+ concentration ([Ca2+]cyt) in pulmonary artery smooth muscle cells (PASMC) is a major trigger for pulmonary vasoconstriction, while increased release of mitogenic factors, upregulation (or downregulation) of ion channels and transporters, and abnormalities in intracellular signaling cascades are key to the remodeling of the pulmonary vasculature. Changes in the expression, function, and regulation of ion channels in PASMC and pulmonary arterial endothelial cells play an important role in the regulation of vascular tone and development of vascular remodeling. This article will focus on describing the ion channels and transporters that are involved in the regulation of pulmonary vascular function and structure and illustrating the potential pathogenic role of ion channels and transporters in the development of pulmonary vascular disease.

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Expression of CLCN Voltage-gated Chloride Channel Genes in Human Blood Vessels

Cited by 49 publications

References 0 publications

Superoxide Flux in Endothelial Cells via the Chloride Channel-3 Mediates Intracellular Signaling

Superoxide Flux in Endothelial Cells via the Chloride Channel-3 Mediates Intracellular Signaling

ClC-5 chloride channel and kidney stones: what is the link?

Endothelial and Smooth Muscle Cell Ion Channels in Pulmonary Vasoconstriction and Vascular Remodeling

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