Leukocyte and Ion Channel Research Laboratory, School of Health and Biosciences, University of East London, Stratford Campus, Romford Road, London E15 4LZ, UK.
Cell Immunol. 2010;262(1):6-10. doi: 10.1016/j.cellimm.2010.02.001. Epub 2010 Feb 4.
The action of two potent store operated Ca2+ entry (SOCE) inhibitors, ML-9 and GdCl3 on Ca2+ fluxes induced by the pro-inflammatory agonists FMLP, PAF, LTB(4) as well as the receptor-independent stimulus thapsigargin has not been documented in human neutrophils. In this study, ML-9 enhanced both release and subsequent Ca2+ influx in response to agonists whereas it enhanced Ca2+ release by thapsigargin, but inhibited Ca2+ influx. In contrast, 1muM GdCl3 completely inhibited Ca2+ influx in response to thapsigargin, but only partially blocked Ca2+ influx after agonist stimulation. These results strongly suggest a major role for receptor-operated Ca2+ influx in human neutrophils.
尚未在人中性粒细胞中记录到两种强效的储存操作钙(Ca2+)内流(SOCE)抑制剂 ML-9 和 GdCl3 对促炎激动剂 FMLP、PAF、LTB4 以及受体非依赖性刺激物 thapsigargin 诱导的 Ca2+流的作用。在这项研究中,ML-9 增强了对激动剂的释放和随后的 Ca2+内流,而增强了 thapsigargin 的 Ca2+释放,但抑制了 Ca2+内流。相比之下,1μM GdCl3 完全抑制了 thapsigargin 引起的 Ca2+内流,但仅部分阻断了激动剂刺激后的 Ca2+内流。这些结果强烈表明受体操作的 Ca2+内流在人中性粒细胞中起主要作用。