Allard B, Long E, Block E, Zhao X
Department of Animal Science, McGill University, Ste-Anne-de-Bellevue, Québec, Canada.
Can J Vet Res. 1999 Jan;63(1):13-7.
The involvement of both intracellular and extracellular calcium, as well as the activation of protein kinase C (PKC), in phorbol myristate acetate (PMA)-stimulated respiratory burst in bovine neutrophils has been studied. PMA significantly stimulated the superoxide anion production by these cells. The increased production of superoxide anion was inhibited by BAPTA/AM, an intracellular calcium ([Ca2+]i) chelator, but not affected by EGTA, an extracellular calcium ([Ca2+]0) chelator. PMA also induced PKC activation, and a PKC inhibitor, calphostin C, blocked the stimulatory effect of PMA on superoxide anion production by the neutrophils. Therefore, we conclude that PMA-induced respiratory burst in bovine neutrophils is [Ca2+]i- but not [Ca2+]0-dependent, and also requires PKC activation.
已经研究了细胞内和细胞外钙以及蛋白激酶C(PKC)的激活在佛波酯肉豆蔻酸酯乙酸酯(PMA)刺激的牛中性粒细胞呼吸爆发中的作用。PMA显著刺激了这些细胞中超氧阴离子的产生。细胞内钙([Ca2+]i)螯合剂BAPTA/AM抑制了超氧阴离子产生的增加,但细胞外钙([Ca2+]0)螯合剂EGTA对其没有影响。PMA还诱导了PKC的激活,并且PKC抑制剂钙泊三醇C阻断了PMA对中性粒细胞超氧阴离子产生的刺激作用。因此,我们得出结论,PMA诱导的牛中性粒细胞呼吸爆发依赖于[Ca2+]i而非[Ca2+]0,并且还需要PKC的激活。