Andrabi K I, Kaul N, Mudassar S, Dilawari J B, Ganguly N K
Department of Experimental Medicine, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Biochem Med Metab Biol. 1991 Apr;45(2):235-43. doi: 10.1016/0885-4505(91)90026-h.
Superoxide production by human neutrophils was stimulated by rat liver collagen. The stimulation was exponentially related to the collagen concentration, with maximal effect at 150 micrograms/ml. The collagen-induced effect was significantly enhanced by the presence of Ca2+ in the medium. Verapamil--a calcium channel blocker--caused a dose-dependent inhibition of superoxide production by collagen-stimulated neutrophils. Collagen-induced stimulation was associated with a transient rise in cytosolic free Ca2+ independent of the presence of Ca2+ in the medium. Depletion of intracellular calcium caused a significant decrease in superoxide activity; however, replenishment of Ca2+ in the medium significantly overcame the inhibition. These changes were associated with a direct binding of [14C]collagen with the neutrophils. Our data suggest that collagen-neutrophil interaction couples superoxide production with the process of Ca2+ mobilization and that this interaction may play a physiologic role in neutrophil stimulation.
大鼠肝脏胶原蛋白可刺激人中性粒细胞产生超氧化物。这种刺激与胶原蛋白浓度呈指数关系，在150微克/毫升时效果最佳。培养基中Ca2+的存在显著增强了胶原蛋白诱导的效应。维拉帕米——一种钙通道阻滞剂——对胶原蛋白刺激的中性粒细胞产生超氧化物具有剂量依赖性抑制作用。胶原蛋白诱导的刺激与胞质游离Ca2+的短暂升高有关，且与培养基中Ca2+的存在无关。细胞内钙的耗尽导致超氧化物活性显著降低；然而，培养基中Ca2+的补充显著克服了这种抑制作用。这些变化与[14C]胶原蛋白与中性粒细胞的直接结合有关。我们的数据表明，胶原蛋白-中性粒细胞相互作用将超氧化物的产生与Ca2+动员过程联系起来，并且这种相互作用可能在中性粒细胞刺激中发挥生理作用。
