Ion channels in human THP-1 monocytes.
The THP-1 human monocytic leukemia cell line is a useful model of macrophage differentiation. Patch clamp methods were used to identify five types of ion channels in undifferentiated THP-1 monocytes. (i) Delayed rectifier K+ current, IDR, was activated by depolarization to potentials positive to -50 mV, inactivated with a time constant of several hundred msec, and recovered from inactivation with a time constant approximately21 sec. IDR was inhibited by 4-aminopyridine (4-AP), tetraethylammonium (TEA+), and potently by charybdotoxin (ChTX). (ii) Ca-activated K+ current (ISK) dominated whole-cell currents in cells studied with 3-10 micron [Ca2+]i. ISK was at most weakly voltage-dependent, with reduced conductance at large positive potentials, and was inhibited by ChTX and weakly by TEA+, Cs+, and Ba2+, but not 4-AP or apamin. Block by Cs+ and Ba2+ was enhanced by hyperpolarization. (iii) Nonselective cation current, Icat, appeared at voltages above +20 mV. Little time-dependence was observed, and a panel of channel blockers was without effect. (iv) Chloride current, ICl, was present early in experiments, but disappeared with time. (v) Voltage-activated H+ selective current is described in detail in a companion paper (DeCoursey & Cherny, 1996. J. Membrane Biol. 152:2). The ion channels in THP-1 cells are compared with channels described in other macrophage-related cells. Profound changes in ion channel expression that occur during differentiation of THP-1 cells are described in a companion paper (DeCoursey et al., 1996. J. Membrane Biol. 152:2).
Kim
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Department of Medicine, Pulmonary Division, Rush Presbyterian St. Luke's Medical Center, 1653 West Congress Parkway, Chicago, IL 60612, USA.
Silver
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DeCoursey
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D015761:4-Aminopyridine / Q000494:pharmacology; D001030:Apamin / Q000494:pharmacology; D002118:Calcium / Q000494:pharmacology; D002413:Cations, Divalent / Q000494:pharmacology; D018999:Charybdotoxin / Q000494:pharmacology; D018118:Chloride Channels / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D015640:Ion Channel Gating / Q000187:drug effects; D007473:Ion Channels / Q000187:drug effects / Q000378:metabolism*; D007948:Leukemia, Monocytic, Acute / Q000378:metabolism / Q000473:pathology*; D009000:Monocytes / Q000187:drug effects / Q000502:physiology*; D009363:Neoplasm Proteins / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism; D024642:Potassium Channels, Voltage-Gated; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D014407:Tumor Cells, Cultured
D002413:Cations, Divalent; D018118:Chloride Channels; D007473:Ion Channels; D009363:Neoplasm Proteins; D015221:Potassium Channels; D024642:Potassium Channels, Voltage-Gated; D013757:Tetraethylammonium Compounds; C087375:charybdotoxin receptor; C059983:potassium channel protein I(sk); D018999:Charybdotoxin; D001030:Apamin; D019789:Tetraethylammonium; D015761:4-Aminopyridine; D011188:Potassium; D002118:Calcium