Ng J, Fredholm B, Jondal M, Andersson T
Int J Immunopharmacol. 1987;9(1):17-22. doi: 10.1016/0192-0561(87)90106-8.
Stimulation of the T-cell line JURKAT with PHA or anti-T3 antibody leads to a rapid and sustained rise of cytosolic free Ca2+, as determined by quin2 fluorescence measurements. Pertussis toxin and N-ethylmaleimide, substances known to inactivate a regulatory N-protein, caused partial to complete inhibition of the cytosolic free Ca2+ response induced both by anti-T3 or PHA. The high cytosolic free Ca2+ level induced by anti-T3 or PHA declined more rapidly after addition of phorbol ester, phorbol myristate acetate (PMA). PMA did not affect cytosolic free Ca2+ changes induced by ionomycin indicating that the effect of PMA is due to a direct inhibitory effect on a transduction mechanism and not to activation of Ca2+ extrusion. Our data suggest that a regulatory N-protein is involved in the transduction of the PHA and anti-T3 response into a rapid and sustained elevation of cytosolic free Ca2+. Activation of protein kinase C by PMA modulates the calcium response in JURKAT cells, suggesting that protein kinase C may be involved in feedback regulation of the transduction mechanism.
用PHA或抗T3抗体刺激T细胞系JURKAT，通过quin2荧光测量法测定，可导致胞质游离Ca2+迅速且持续升高。百日咳毒素和N-乙基马来酰亚胺是已知能使一种调节性N蛋白失活的物质，它们会部分或完全抑制由抗T3或PHA诱导的胞质游离Ca2+反应。添加佛波酯（佛波醇肉豆蔻酸酯乙酸酯，PMA）后，由抗T3或PHA诱导的高胞质游离Ca2+水平下降得更快。PMA不影响离子霉素诱导的胞质游离Ca2+变化，这表明PMA的作用是由于对转导机制的直接抑制作用，而不是由于Ca2+外流的激活。我们的数据表明，一种调节性N蛋白参与了将PHA和抗T3反应转导为胞质游离Ca2+迅速且持续升高的过程。PMA激活蛋白激酶C可调节JURKAT细胞中的钙反应，这表明蛋白激酶C可能参与了转导机制的反馈调节。
