

Other version: http://www.jbc.org/content/264/13/7251.full.pdf
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Chemoattractant receptor promotion of Ca2+ influx across the plasma membrane of HL-60 cells. A role for cytosolic free calcium elevations and inositol 1,3,4,5-tetrakisphosphate production |
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Published in | The Journal of biological chemistry. 1989, vol. 264, no. 13, p. 7251-7261 | |
Abstract | The mechanisms by which the chemotactic peptide formyl-methyl-leucyl-phenyl-alanine stimulates Ca2+ influx across the plasma membrane were investigated in the human promyelocytic cell line HL-60, induced to differentiate with dimethyl sulfoxide. Ca2+ influx was determined: (a) from the initial rate of Mn2+ influx, apparent from the quenching of intracellular quin2 or fura-2 fluorescence; (b) from the rate of the elevation of cytosolic free calcium, [Ca2+]i, upon readdition of Ca2+ to cells previously stimulated in the absence of extracellular Ca2+. [3H]Inositol tris-, tetrakis-, and pentakisphosphates were analyzed by a high performance liquid chromatography procedure which was optimized for the separation of inositol tetrakisphosphates, yielding three predominant isomers: inositol 1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P4), inositol 1,4,5,6-tetrakisphosphate, and inositol 1,3,4, 6-tetrakisphosphate. Both the kinetics and agonist dose dependence of Ca2+ influx stimulation correlated closely with the corresponding receptor-mediated variations of [Ca2+]i either in the presence or in the absence of extracellular Ca2+. Of the different inositol phosphates determined in parallel and under the same conditions, accumulation of [3H]Ins(1,3,4,5)P4 correlated best with Ca2+ influx both temporally and in its dose dependence in the presence or in the absence of extracellular Ca2+; inositol 1,3,4-trisphosphate was also correlated but to a lesser extent. Attenuations of [Ca2+]i elevations by decreasing extracellular Ca2+ or by increasing the cytosolic Ca2+ buffering capacity with quin2 led to parallel inhibition of Ca2+ influx and Ins(1,3,4,5)P4 production. In conclusion: 1) activation of Ca2+ influx by formyl-methionyl-leucyl-phenylalanine depends on the elevation of [Ca2+]i, the latter being initiated by Ca2+ mobilization from intracellular stores; 2) Ins(1,3, 4,5)P4 is a strong candidate for maintaining receptor-mediated activation of Ca2+ influx in differentiated HL-60 cells. | |
Keywords | Aminoquinolines/pharmacology — Biological Transport — Calcium/ physiology — Calcium Channels/physiology — Cell Membrane/ metabolism — Dose-Response Relationship, Drug — Humans — Inositol Phosphates/ physiology — Isomerism — Kinetics — Leukemia, Promyelocytic, Acute — Microscopy, Fluorescence — N-Formylmethionine Leucyl-Phenylalanine/ pharmacology — Neutrophils/ physiology — Sugar Phosphates/ physiology — Tumor Cells, Cultured | |
Identifiers | PMID: 2540183 | |
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Research group | Staphylocoques dorés résistants à la méthicilline et hygiène hospitalière (330) | |
Citation (ISO format) | PITTET, Didier et al. Chemoattractant receptor promotion of Ca2+ influx across the plasma membrane of HL-60 cells. A role for cytosolic free calcium elevations and inositol 1,3,4,5-tetrakisphosphate production. In: The Journal of biological chemistry, 1989, vol. 264, n° 13, p. 7251-7261. doi: 10.1016/S0021-9258(18)83228-8 https://archive-ouverte.unige.ch/unige:7508 |