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PH Naccache, AC Caon, C Gilbert, G Chouinard and SR McColl
Department of Medicine, Universite Laval, Ste Foy, Quebec, Canada.
The effects of pertussis toxin (PT) on the growth and dimethylsulfoxide
(Me2SO4)-induced differentiation of the HL-60 human promyelocytic leukemia
cell line were tested. Cell growth was quantified by direct cell counts.
Cell differentiation was estimated by measuring the expression of
myeloid-specific cell-surface antigens (Mo-1 and fMet-Leu- Phe [fMLP]
receptors), the ability of the cells to produce superoxide anions on
stimulation with fMLP, the calcium ionophore A23187 and phorbol
12-myristate 13-acetate (PMA), and by monitoring the level of expression of
messenger RNA (mRNA) for tumor necrosis factor alpha (TNF alpha). By
itself, PT did not affect the proliferation of HL-60 cells in
serum-containing medium. In contrast, PT (but not its B-oligomer)
dose-dependently inhibited the Me2SO4-induced expression of Mo-1, fMLP
receptors, and the oxidative responses to the chemotactic factor and to
A23187, but not to PMA. The addition of Me2SO4 induced a significant
increase in the steady-state levels of TNF alpha mRNA, and this effect was
strongly inhibited by PT. Finally, the bacterial toxin did not reverse the
block of cell division that follows the addition of Me2SO4. These results
provide evidence for the involvement of a PT substrate (presumably a
guanine nucleotide-binding protein) in the regulation of the maturation of
the excitation-response coupling sequence in human myeloid cell precursors
and show that the regulation of cell division and maturation of HL-60 cells
are under distinct sets of control mechanisms.
This article has been cited by other articles:
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| Copyright © 1991 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
