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  • Title: Stimulatory and inhibitory guanine-nucleotide-binding regulatory protein involvement in stimulation of arachidonic-acid release by N-formyl-methionyl-leucyl-phenylalanine and platelet-activating factor from guinea-pig alveolar macrophages. Differential receptor/G-protein interaction assessed by pertussis and cholera toxins.
    Author: Levistre R, Masliah J, Bereziat G.
    Journal: Eur J Biochem; 1993 Apr 01; 213(1):295-303. PubMed ID: 8386624.
    Abstract:
    The involvement of guanine-nucleotide-binding regulatory proteins (G proteins) in the regulation of arachidonic-acid release induced by N-formyl-methionyl-leucyl-phenylalanine (fMet-Leu-Phe) or platelet-activating factor (PAF) was examined in guinea-pig alveolar macrophages. We report that maximal release of arachidonic acid in permeabilized cells requires the simultaneous addition of the agonist (fMet-Leu-Phe or PAF) and of GTP (or GTP[S]). Prior treatment of cells with increasing concentrations of pertussis toxin induces a parallel decrease of arachidonic-acid release and of the labeling of a 40-kDa protein in membranes incubated with [32P]NAD and pertussis toxin. fMet-Leu-Phe, but not PAF, allows the ADP-ribosylation of a 40-KDa protein by cholera toxin in the presence of Mg2+. This effect is prevented by guanyl nucleotides and by prior treatment with pertussis toxin. The 40-kDa protein ADP-ribosylated seems to be alpha i1 and/or alpha i2. Stimulation of GTPase activity by fMet-Leu-Phe and PAF has the same amplitude and is completely inhibited by pertussis toxin, but only in part by cholera toxin. Prior treatment of alveolar macrophages with cholera toxin, which ADP-ribosylates Gs, inhibits PAF-stimulated and fMet-Leu-Phe-stimulated arachidonic-acid release to the same extent, via a cAMP-protein-kinase-A cascade. The decreased responsiveness of alveolar macrophages previously treated with cholera toxin to fMet-Leu-Phe and PAF is associated with a strong increase of in-vitro [32P]NAD labeling of Gi proteins either by pertussis or by cholera toxin. This effect is mimicked by prior treatment of the cells with dibutyryl cAMP and okadaic acid, a protein-phosphatase inhibitor, suggesting the involvement of protein-kinase A in this process. In conclusion, our results demonstrate that fMet-Leu-Phe and PAF receptors interact differently with Gi1/2 proteins in guinea-pig alveolar macrophages. Gi1/2 proteins are a possible target of the cross-regulation of arachidonic-acid release by a Gs-mediated pathway.
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