Pongracz J, Lord J M
Department of Immunology, University of Birmingham, United Kingdom.
Biochem Biophys Res Commun. 1998 Jun 29;247(3):624-9. doi: 10.1006/bbrc.1998.8867.
Selective protein kinase C (PKC) activators and inhibitors and a physiological agonist, fMLP, were used to study superoxide production and PKC isoenzyme activation in human neutrophils. The data show that the classical PKC isoenzymes, alpha and beta, were activated by TPA and at a time prior to NADPH oxidase complex assembly. fMLP induced activation of PKC-beta over a similar time course. Inhibition of c-PKCs reduced, but did not block, TPA-induced superoxide production completely, suggesting additional PKC isoenzymes were involved beyond NADPH oxidase assembly. PKC inhibitors were unable to inhibit fMLP-induced superoxide generation, indicative of signal redundancy in the induction of superoxide generation in human neutrophils.
选用选择性蛋白激酶C（PKC）激活剂、抑制剂以及一种生理性激动剂fMLP，来研究人中性粒细胞中超氧化物的产生及PKC同工酶的激活情况。数据显示，经典PKC同工酶α和β可被佛波酯（TPA）激活，且在NADPH氧化酶复合物组装之前的某个时间点被激活。fMLP在相似的时间进程中诱导PKC-β的激活。抑制经典PKC（c-PKCs）可减少但不能完全阻断TPA诱导的超氧化物产生，这表明除了NADPH氧化酶组装外，还有其他PKC同工酶参与其中。PKC抑制剂无法抑制fMLP诱导的超氧化物生成，这表明人中性粒细胞中超氧化物生成诱导过程存在信号冗余。
