O'Flaherty J T, Cousart S, Swendsen C L, DeChatelet L R, Bass D A, Love S H, McCall C E
Biochim Biophys Acta. 1981 Jan 8;640(1):223-30. doi: 10.1016/0005-2736(81)90547-2.
The influence of extracellular Ca2+ and Mg2+ on the transport of 2-deoxy-[3H]glucose into human polymorphonuclear neutrophils was studied. Omission of these cations from the cell suspensions had little effect on resting hexose uptake. Furthermore, the addition of the bivalent cation chelator, EDTA, depressed uptake only slightly. Similarly, neither cation was essential for the enhanced 2-deoxy-D-[3H]glucose uptake stimulated by two chemotactic factors (C5a and N-formylmethionylleucylphenylalanine) and arachidonic acid: enhanced uptake was only partially depressed by the omission of Ca2+ and Mg2+ from the suspensions and was still prominent in the presence of EDTA. Two other neutrophil stimulants, the ionophores, A23187 and ionomycin, also enhanced hexose uptake but their actions were heavily dependent upon extracellular bivalent cations and were totally abrogated by EDTA. In all instances, extracellular Ca2+, but not Mg2+, supported optimal enhanced hexose transport induced by stimuli. Activation of 2-deoxy-D-[3H]glucose uptake by each of the five stimuli was totally blocked by cytochalasin B (a blocker of carrier-mediated hexose transport) and D-glucose but not by L-glucose. The data indicate, therefore, that a variety of neutrophil stimulants activate carrier-mediated hexose transport. Although this transport can be triggered by the movement of extracellular Ca2+ into the cell (as exemplified by the action of the two ionophores), such Ca2+ movement is not required for the actions of chemotactic factors or arachidonic acid. Other mechanisms, such as a rearrangement of intracellular Ca2+, may be involved in mediating the activation of hexose transport induced by the latter stimuli.
研究了细胞外钙离子（Ca2+）和镁离子（Mg2+）对2-脱氧-[3H]葡萄糖转运进入人多形核中性粒细胞的影响。从细胞悬液中去除这些阳离子对静息状态下己糖摄取的影响很小。此外，添加二价阳离子螯合剂乙二胺四乙酸（EDTA）仅轻微降低摄取。同样，这两种阳离子对于由两种趋化因子（C5a和N-甲酰甲硫氨酰亮氨酰苯丙氨酸）和花生四烯酸刺激引起的2-脱氧-D-[3H]葡萄糖摄取增强也不是必需的：通过从悬液中去除Ca2+和Mg2+，摄取增强仅部分受到抑制，并且在EDTA存在下仍然显著。另外两种中性粒细胞刺激剂，离子载体A23187和离子霉素，也增强了己糖摄取，但它们的作用严重依赖于细胞外二价阳离子，并且被EDTA完全消除。在所有情况下，细胞外Ca2+而非Mg2+支持由刺激诱导的最佳己糖转运增强。细胞松弛素B（载体介导的己糖转运阻滞剂）和D-葡萄糖完全阻断了五种刺激物中每种对2-脱氧-D-[3H]葡萄糖摄取的激活，而L-葡萄糖则不能。因此，数据表明，多种中性粒细胞刺激剂激活载体介导的己糖转运。尽管这种转运可以由细胞外Ca2+进入细胞的运动触发（如两种离子载体的作用所示），但趋化因子或花生四烯酸的作用并不需要这种Ca2+运动。其他机制，如细胞内Ca2+的重排，可能参与介导后一种刺激物诱导的己糖转运激活。
