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Macrophage‐colony‐stimulating factor (CSF‐1) modulates a differentiation‐specific inward‐rectifying potassium current in human leukemic (HL‐60) cells
Author(s) -
Wieland Steven J.,
Chou Robin H.,
Gong QiHua
Publication year - 1990
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041420326
Subject(s) - extracellular , intracellular , hyperpolarization (physics) , phorbol , microbiology and biotechnology , macrophage , chemistry , potassium channel , biophysics , patch clamp , inward rectifier potassium ion channel , biology , biochemistry , ion channel , in vitro , protein kinase c , signal transduction , receptor , stereochemistry , nuclear magnetic resonance spectroscopy
A voltage‐activated inward‐rectifying K + conductance (I ki ) appears in human promyelocytic leukemia (HL‐60) cells during phorbol ester‐induced differentiation into macrophages. This conductance was detected in the cells 24 hours after exposure to phorbol‐12‐myristate‐13‐acetate (PMA), as the cells began to express the macrophage phenotype, and continued to increase for 4 days after PMA exposure. The magnitude of inward current was a function of external K + ; current was blocked by extracellular or intracellular Cs + and by extracellular Ba ++ . Hyperpolarization produced activation at membrane potentials more negative than −80 mV, and a slower, partial inactivation also occurred at potentials more negative than −100 mV. This conductance was not detected in proliferating cells nor in granulocytes derived from HL‐60 cells which were induced to differentiate with retinoic acid (RA). Exposure of differentiated macrophages to recombinant human CSF‐1 produced inhibition of the I ki beginning within 1 minute after exposure. CSF‐1 inhibition of I ki channels in cell‐attached patches indicated that channel modulation was via intracellular mediators. The rapid inhibition of the inward rectifier by the macrophage‐specific CSF‐1 appears to be one of the earliest cellular responses to this factor.