VCAM-1-induced inwardly rectifying K(+) current enhances Ca(2+) entry in human THP-1 monocytes |
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Authors: | Colden-Stanfield M Scanlon M |
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Institution: | Department of Physiology, Morehouse School of Medicine, Atlanta, Georgia 30310, USA. stanfiel@msm.edu |
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Abstract: | Hyperpolarization in human leukemia THP-1 monocytes adherent tovascular cell adhesion molecule (VCAM)-1 is due to an induction ofinwardly rectifying K+ currents(Iir) (Colden-Stanfield M and Gallin EK,Am J Physiol Cell Physiol 275: C267-C277, 1998).We determined whether the VCAM-1-induced hyperpolarization issufficient to augment the increase in intracellular free calcium(Ca2+]i) produced by Ca2+ storedepletion with thapsigargin (TG) and readdition of external CaCl2 in fura 2-loaded THP-1 monocytes. Whereas there was a2.1-fold increase in Ca2+]i in monocytesbound to glass for 5 h in response to TG and CaCl2 addition, adherence to VCAM-1 produced a 5-fold increase inCa2+]i. Depolarization of monocytes adherentto VCAM-1 by Iir blockade or exposure to highK+] abolished the enhancement of the peakCa2+]i response. In monocytes bound toglass, hyperpolarization of the membrane potential with valinomycin, aK+ ionophore, to the level of hyperpolarization seen incells adherent to VCAM-1 produced similar changes in peakCa2+]i. Adherence of monocytes to E-selectinproduced a similar peak Ca2+]i to cellsbound to glass. Thus monocyte adherence to the physiological substrateVCAM-1 produces a hyperpolarization that is sufficient to enhanceCa2+ entry and may impact Ca2+-dependentmonocyte function. |
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