Davis W, Halliwell E L, Sage S O, Allen J M
Physiological Laboratory, University of Cambridge, UK.
Cell Calcium. 1995 May;17(5):345-53. doi: 10.1016/0143-4160(95)90108-6.
We have investigated the mechanisms underlying calcium signalling evoked by cross-linking of the high affinity IgG receptor (Fc gamma RI) in populations of the human monocyte-like cell line, U937, following activation of the cells by cytokine treatment, or differentiation to a more macrophage-like state by treatment with dibutyryl cAMP (Bt2cAMP). We have shown previously that a larger and more prolonged entry of external calcium occurs in Bt2cAMP-differentiated cells, although there is a smaller initial release from internal stores in these cells than in those activated by IFN-gamma treatment. In this paper we demonstrate, by use of the endomembrane Ca(2+)-ATPase inhibitor, thapsigargin, that this effect is explained (at least in part) by an enhanced capacity for store regulated entry of calcium in Bt2cAMP-differentiated cells.
我们研究了在人单核细胞样细胞系U937中,通过细胞因子处理激活细胞或用二丁酰环磷腺苷(Bt2cAMP)处理使其分化为更类似巨噬细胞的状态后,高亲和力IgG受体(FcγRI)交联引发钙信号传导的潜在机制。我们之前已经表明,尽管与经干扰素-γ处理激活的细胞相比,Bt2cAMP分化细胞从内部储存库释放的初始钙量较少,但外部钙的进入量更大且持续时间更长。在本文中,我们通过使用内膜Ca(2+)-ATP酶抑制剂毒胡萝卜素证明,这种效应(至少部分)是由于Bt2cAMP分化细胞中储存调节性钙进入能力增强所致。