Christiansen N O
Department of Medicine and Infectious Diseases, Marselisborg Hospital, University of Aarhus, Denmark.
J Leukoc Biol. 1990 Jan;47(1):60-3. doi: 10.1002/jlb.47.1.60.
The effect of pertussis toxin on N-formyl-methionyl-leucyl-phenylalanine (FMLP), phorbol 12-myristate 13-acetate (PMA), ionomycin, and A23187-induced translocation of protein kinase C and superoxide generation was studied in human neutrophils. Pertussis toxin was shown to inhibit FMLP-induced superoxide generation in parallel with an inhibition of protein kinase C translocation. In contrast, no effect of pertussis toxin was demonstrated upon superoxide generation or protein kinase C translocation in PMA-, A23187-, or ionomycin-stimulated cells. In that superoxide generation and protein kinase C translocation were inhibited in parallel, it is concluded that a G-protein-dependent cascade is involved in the FMLP-induced activation of protein kinase C, and this cascade may be equivalent to the pathway inducing superoxide generation.
在人中性粒细胞中研究了百日咳毒素对N-甲酰甲硫氨酰亮氨酰苯丙氨酸（FMLP）、佛波酯12-肉豆蔻酸酯13-乙酸酯（PMA）、离子霉素和A23187诱导的蛋白激酶C易位及超氧化物生成的影响。结果显示，百日咳毒素在抑制FMLP诱导的超氧化物生成的同时，也抑制了蛋白激酶C的易位。相比之下，在PMA、A23187或离子霉素刺激的细胞中，未观察到百日咳毒素对超氧化物生成或蛋白激酶C易位有影响。由于超氧化物生成和蛋白激酶C易位被同时抑制，因此得出结论，G蛋白依赖性级联反应参与了FMLP诱导的蛋白激酶C激活，并且该级联反应可能等同于诱导超氧化物生成的途径。
