Macrophage‐colony‐stimulating factor (CSF‐1) modulates a differentiation‐specific inward‐rectifying potassium current in human leukemic (HL‐60) cells

Wieland, Steven J.; Chou, Robin H.; Gong, Qiong

doi:10.1002/jcp.1041420326

Cited by 26 publications

(9 citation statements)

References 37 publications

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“…Given the functional similarities between macrophages and neutrophils, as well as their derivation from a common precursor, it seems plausible that they would be similar in their ion channel expression profile. However, the human promyelocytic cell line HL-60 expresses Kir2 channels when it is differentiated into macrophages but not into granulocytes (56), possibly indicating that there are important differences in ion channel expression between the two phagocytic lineages in humans.…”

Section: C272 Kir21 Channels In Mouse Neutrophilsmentioning

confidence: 99%

The inward rectifier potassium channel Kir2.1 is expressed in mouse neutrophils from bone marrow and liver

Masia

Krause

Yellen

2015

American Journal of Physiology-Cell Physiology

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Neutrophils are phagocytic cells that play a critical role in innate immunity by destroying bacterial pathogens. Channels belonging to the inward rectifier potassium channel subfamily 2 (Kir2 channels) have been described in other phagocytes (monocytes/macrophages and eosinophils) and in hematopoietic precursors of phagocytes. Their physiological function in these cells remains unclear, but some evidence suggests a role in growth factor-dependent proliferation and development. Expression of functional Kir2 channels has not been definitively demonstrated in mammalian neutrophils. Here, we show by RT-PCR that neutrophils from mouse bone marrow and liver express mRNA for the Kir2 subunit Kir2.1 but not for other subunits (Kir2.2, Kir2.3, and Kir2.4). In electrophysiological experiments, resting (unstimulated) neutrophils from mouse bone marrow and liver exhibit a constitutively active, external K+-dependent, strong inwardly rectifying current that constitutes the dominant current. The reversal potential is dependent on the external K+ concentration in a Nernstian fashion, as expected for a K+-selective current. The current is not altered by changes in external or internal pH, and it is blocked by Ba2+, Cs+, and the Kir2-selective inhibitor ML133. The single-channel conductance is in agreement with previously reported values for Kir2.1 channels. These properties are characteristic of homomeric Kir2.1 channels. Current density in short-term cultures of bone marrow neutrophils is decreased in the absence of growth factors that are important for neutrophil proliferation [granulocyte colony-stimulating factor (G-CSF) and stem cell factor (SCF)]. These results demonstrate that mouse neutrophils express functional Kir2.1 channels and suggest that these channels may be important for neutrophil function, possibly in a growth factor-dependent manner.

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Section: C272 Kir21 Channels In Mouse Neutrophilsmentioning

confidence: 99%

The inward rectifier potassium channel Kir2.1 is expressed in mouse neutrophils from bone marrow and liver

Masia

Krause

Yellen

2015

American Journal of Physiology-Cell Physiology

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“…C ell cycle-dependent changes in K ϩ current expression have been studied more directly in a few cell preparations, which provide evidence for a loss of K IR activity during proliferation, consistent with our data. For example, proliferating human leukemia cells generally lack expression of K IR currents, but currents are upregulated rapidly on induction to differentiate into macrophages (Wieland et al, 1990). Mouse embryos (Day et al, 1993), HeLa cells (Takahashi et al, 1994), and neuroblastoma cells (Arcangeli et al, 1995) all exhibit a downregulation of K IR currents on entrance into S-phase of cell cycle.…”

Section: Electrophysiological Changes In Gliosis Mirror Those Associamentioning

confidence: 99%

Electrophysiological Changes That Accompany Reactive GliosisIn Vitro

1997

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An in vitro injury model was used to examine the electrophysiological changes that accompany reactive gliosis. Mechanical scarring of confluent spinal cord astrocytes led to a threefold increase in the proliferation of scar-associated astrocytes, as judged by bromodeoxyuridine (BrdU) labeling. Whole-cell patch-clamp recordings demonstrated that current profiles differed absolutely between nonproliferating (BrdU Ϫ ) and proliferating (BrdU ϩ ) astrocytes. The predominant current type expressed in BrdU Ϫ cells was an inwardly rectifying K ϩ current (K IR ; 1.3 pS/pF). BrdU Ϫ cells also expressed transient outward K ϩ currents, accounting for less than one-third of total K ϩ conductance (G). In contrast, proliferating BrdU ϩ astrocytes exhibited a dramatic, approximately threefold reduction in K IR (0.45 pS/pF) but showed a twofold increase in the conductance of both transient (K A ) (0.67-1.32 pS/pF) and sustained (K D ) (0.42-1.10 pS/pF) outwardly rectifying K ϩ currents, with a G KIR : G KD ratio of 0.4. Relative expression of G KIR :G KD led to more negative resting potentials in nonproliferating (Ϫ60 mV) versus proliferating astrocytes (Ϫ53 mV; p ϭ 0.015). Although 45% of the nonproliferating astrocytes expressed Na ϩ currents (0.47 pS/pF), the majority of proliferating cells expressed prominent Na ϩ currents (0.94 pS/pF). Injury-induced electrophysiological changes are rapid and transient, appearing within 4 hr postinjury and, with the exception of K IR , returning to control conductances within 24 hr. These differences between proliferating and nonproliferating astrocytes are reminiscent of electrophysiological changes observed during gliogenesis, suggesting that astrocytes undergoing secondary, injury-induced proliferation recapitulate the properties of immature glial cells. The switch in predominance from K IR to K D appears to be essential for proliferation and scar repair, because both processes were inhibited by blockade of K D .

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“…Studies have shown the presence of different types of ion channels in blood cells, including inwards and outwards rectifying K channels, mechanosensitive cation channels, Cl and Na channels and a Ca-dependent Na channel regulated by the actin cytoskeleton [2,3,4,5,6].…”

Section: Introductionmentioning

confidence: 99%

An outwardly rectifying anion channel in human leukaemic K562 cells

Assef

Kotsias

2002

Pfl�gers Archiv European Journal of Physiology

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In this study, an outwardly rectifying anion channel was characterized in the cell line K562 obtained from a chronic human leukaemia. Ion channel activity was recorded in the cell-detached (inside-out) configuration with standard patch-clamp technology. In most of the K562 cells studied, the channel exhibited low spontaneous activity, an outwardly rectifying current/voltage relationship and single-channel conductances of 19 pS and 40 pS for inwards and outwards currents respectively. The channel had a low permeability for gluconate with a relative permeability P(gluconate)/ P(Cl) of 0.14 and was blocked by glibenclamide (50 micro M) or diphenylamine-2-carboxylate (DPC, 1 mM) added to the cytoplasmic side of the patch. These results are characteristic of the outwardly rectifying Cl channel (ORCC) found in other types of cells.

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Macrophage‐colony‐stimulating factor (CSF‐1) modulates a differentiation‐specific inward‐rectifying potassium current in human leukemic (HL‐60) cells

Cited by 26 publications

References 37 publications

The inward rectifier potassium channel Kir2.1 is expressed in mouse neutrophils from bone marrow and liver

The inward rectifier potassium channel Kir2.1 is expressed in mouse neutrophils from bone marrow and liver

Electrophysiological Changes That Accompany Reactive GliosisIn Vitro

An outwardly rectifying anion channel in human leukaemic K562 cells

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