An outwardly rectifying anion channel in human leukaemic K562 cells

Assef, Yanina Andrea; Kotsias, Basilio A.

doi:10.1007/s00424-002-0891-0

Cited by 10 publications

(9 citation statements)

References 34 publications

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“…As for ORCC described in HT29 cells, 19 the human atrial channel was inhibited by NPPB in the range of 1–10 μM. Also, in leukaemic K262 cells as in M‐1 mouse cortical collecting duct cells, the channel is inhibited by glibenclamide 14,18 . The IC 50 value obtained by those authors is close to that estimated here for human atrial ORCCs (40 μM vs 21.5 μM).…”

Section: Discussionsupporting

confidence: 83%

“…The conductance, pharmacology, and rectification properties of the channel resemble those of outwardly rectifying chloride channels previously described in a variety of excitable and nonexcitable tissues, including the heart (for review, see reference 1). In particular, such channels were reported to be present in human cell lines that include intestinal, bronchial, and leukaemic K262 cells 16–18 …”

Section: Discussionmentioning

confidence: 99%

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An Outwardly Rectifying Chloride Channel in Human Atrial Cardiomyocytes

Demion

Guinamard

Chemaly

et al. 2006

Cardiovasc electrophysiol

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Section: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 99%

An Outwardly Rectifying Chloride Channel in Human Atrial Cardiomyocytes

Demion

Guinamard

Chemaly

et al. 2006

Cardiovasc electrophysiol

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“…Surprising, ORCCs in those different cardiac tissues are similar in terms of their outward rectifying properties, I-V curves, and modulation by ATP, which suggests that ORCCs are ubiquitously expressed in the cardiovascular system and may have similar molecular composition. The conductance of cardiovascular ORCCs we recorded here was ϳ90 -100 pS at positive potential range (ϩ40 to ϩ80 mV), which is slightly larger than that of atrial ORCCs reported previously (ϳ60 -76 pS) (5, 10) and much larger than noncardiac ORCCs (40 -50 pS) (1,13,26). Thus there appears to be tissue-specific diversity in the properties of ORCC.…”

Section: CLcontrasting

confidence: 59%

“…A subset of Cl Ϫ channels exist that have been identified at the single-channel level with an outwardly rectifying Cl Ϫ current (ORCC) in symmetrical Cl Ϫ solution. These channels are widely distributed and have been found in many different tissues including human neurocytes (2), airway epithelium (26), lymphocytes (13), and leukemia cells (1) and in rabbit and human atrial myocytes (5, 9, 10). Since volume-regulated anion current (VRAC) and ORCC share many similarities in biophysical properties, ORCC was thought to be, at least in part, responsible for VRAC in atrial myocytes (5,9), which may be an important potential therapeutic target for the treatment of heart disease (3).…”

mentioning

confidence: 99%

Modulation of human cardiovascular outward rectifying chloride channel by intra- and extracellular ATP

Liu¹,

Vepa²,

Artman³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Liu GX, Vepa S, Artman M, Coetzee WA. Modulation of human cardiovascular outward rectifying chloride channel by intra-and extracellular ATP. Am J Physiol Heart Circ Physiol 293: H3471-H3479, 2007. First published October 12, 2007; doi:10.1152/ajpheart.00357.2007.-The macroscopic volume-regulated anion current (VRAC) is regulated by both intracellular and extracellular ATP, which has important implications in signaling and regulation of cellular excitability. The outwardly rectifying Cl Ϫ channel (ORCC) is a major contributor to the VRAC. This study investigated the effects of intracellular and extracellular ATP on the ORCCs expressed in the human cardiovascular system. With inside-out singlechannel patch-clamp techniques, ORCCs were recorded from myocytes isolated from human atrium and septal ventricle and from primary cells originating from human coronary artery endothelium and human coronary artery smooth muscle. ORCCs from all of these tissues had similar biophysical properties, i.e., they were outwardly rectifying in symmetrical Cl Ϫ solutions, exhibited a slope conductance of ϳ90 -100 pS at positive potentials and ϳ22 pS at negative potentials, and had a high open probability that was independent of voltage or time. The presence of ATP at the cytosolic face of the membrane increased the number of patches that contained functional ORCC but had no effect on gating. In contrast, "extracellular" ATP (in pipette solution) had no effect on the proportion of patches in which ORCC was detected but strongly reduced the open probability by increasing the closed dwell time. The potency order for nucleotides to affect gating was ATP␥S Ͼ ATP ϭ UTP Ͼ ADP Ͼ AMP, which suggests that a negatively charged phosphate group is involved in ORCC block. Our findings are consistent with a role of ORCC in the human cardiovasculature (atrium, ventricle, and coronary arteries). Regulation of ORCC by extracellular ATP suggests that this channel may have an important role in maintaining electrical activity and membrane potential under conditions in which extracellular ATP levels are elevated, such as with ATP release from nerve endings or during pathophysiological conditions. human heart; atrial myocytes; ventricular myocytes; endothelial cells; smooth muscle cells CHLORIDE CHANNELS in the cardiovascular system play an important role in maintaining the resting potential and by participating in repolarization of the action potential (15,17,27). There are several types of macroscopic Cl Ϫ currents identified by whole cell patch-clamp recordings, which are distinguished from each other in terms of their regulation. These include Cl

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“…K562 cells also express cystic fibrosis transmembrane regulator (CFTR) mRNA transcripts (51) and P-glycoprotein (50). According to this, we recently reported (3) in K562 cells the presence of an anionic channel with an outward rectification (ORCC), a channel regulated by the CFTR (21,37).…”

mentioning

confidence: 99%

CFTR in K562 human leukemic cells

Assef

Damiano

Zotta

et al. 2003

American Journal of Physiology-Cell Physiology

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In this study, the expression and functional characterization of CFTR (cystic fibrosis transmembrane regulator) was determined in K562 chronic human leukemia cells. Expression of the CFTR gene product was determined by RT-PCR and confirmed by immunohistochemistry and Western blot analysis. Functional characterization of CFTR Cl- channel activity was conducted with patch-clamp techniques. Forskolin, an adenylyl cyclase activator, induced an anion-selective channel with a linear current-voltage relationship and a single-channel conductance of 11 pS. This cAMP-activated channel had a Pgluconate/PCl or PF/PCl perm-selectivity ratio of 0.35 and 0.30, respectively, and was inhibited by the CFTR blocker glibenclamide and the anti-CFTR antibody MAb 13-1, when added to the cytoplasmatic side of the patch. Glibenclamide decreased the open probability increasing the frequency of open-to-closed transitions. Addition of 200 μM DIDS caused an irreversible block of the channels when added to the cytosolic side of inside-out patches. These and other observations indicate a widespread distribution of CFTR gene expression and suggest that this channel protein may function in most human cells to help maintain cellular homeostasis.

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An outwardly rectifying anion channel in human leukaemic K562 cells

Cited by 10 publications

References 34 publications

An Outwardly Rectifying Chloride Channel in Human Atrial Cardiomyocytes

An Outwardly Rectifying Chloride Channel in Human Atrial Cardiomyocytes

Modulation of human cardiovascular outward rectifying chloride channel by intra- and extracellular ATP

CFTR in K562 human leukemic cells

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