Stimulation by leukotriene D4 of increases in the cytosolic concentration of calcium in dimethylsulfoxide-differentiated HL-60 cells.
Stimulation by leukotriene D4 of increases in the cytosolic concentration of calcium in dimethylsulfoxide-differentiated HL-60 cells.
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白三烯 D4 刺激二甲亚砜分化的 HL-60 细胞中胞浆钙浓度增加。
DOI：
10.1172/jci113192
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
Koo,CH
中科院分区：
文献类型：
--
作者：
Baud,L;Goetzl,EJ;Koo,CH
c6 -硫肽白三烯C4 （LTC4）和D4 （LTD4）引起二甲亚砜分化HL-60细胞胞内钙（[Ca+2]i）浓度升高，通过quin-2荧光检测。[Ca+2]i的增加在15 ~ 90 s内达到峰值，在1.2 nM LTD4和60 nM LTC4处达到最大水平的50%，LTD4的最大幅度大于LTC4，并在5 ~ 7 min内消退。流式细胞术评估ltd4诱导的[Ca+2]i的增加，反映在细胞内indo-1荧光的增加，显示平均77%的分化HL-60细胞有反应，而未分化的HL-60细胞只有50%有较小的增加。用LTD4预处理HL-60细胞能够阻止[Ca+2]i对LTC4和LTD4的后续反应，并且发现LTC4转化为LTD4的丝氨酸硼酸盐抑制剂同时抑制LTC4诱导的[Ca+2]i升高和对Sephadex G-25的粘附性增加，这表明HL-60细胞对LTC4的反应需要转化为LTD4。百日咳毒素和LTD4的化学拮抗剂降低了[Ca+2]i的反应，这表明对LTD4受体的依赖。ltd4诱导的[Ca+2]i的增加依赖于细胞外钙，并被镧减少，但不受硝苯地平的影响，也不与膜电位的变化相关，用荧光探针3,3'-二戊基氧碳蓝测定。因此，HL-60细胞中[Ca+2]i的增加与粘附性的增加相结合，似乎与质膜中LTD4受体特异性和电压无关的钙通道有关。
The C6-sulfidopeptide leukotrienes C4 (LTC4) and D4 (LTD4) evoked increases in the cytosolic concentration of intracellular calcium ([Ca+2]i) in dimethylsulfoxide-differentiated HL-60 cells, as assessed by the fluorescence of quin-2. The increases in [Ca+2]i reached a peak within 15-90 s, attained 50% of the maximum level at 1.2 nM LTD4 and 60 nM LTC4, were greater in maximal magnitude for LTD4 than LTC4, and subsided in 5-7 min. Flow cytometric evaluation of the LTD4-induced increases in [Ca+2]i, reflected in increases in the fluorescence of intracellular indo-1, revealed that a mean of 77% of differentiated HL-60 cells responded, as contrasted with lesser increases in only 50% of undifferentiated HL-60 cells. The capacity of pretreatment of HL-60 cells with LTD4 to prevent subsequent responses of [Ca+2]i to LTC4 and LTD4, and the finding that the serine-borate inhibitor of conversion of LTC4 to LTD4 suppressed concurrently both LTC4-induced rises in [Ca+2]i and increases in adherence to Sephadex G-25 indicated that the responses of HL-60 cells to LTC4 required conversion to LTD4. That pertussis toxin and a chemical antagonist of LTD4 reduced the [Ca+2]i response suggested a dependence on LTD4 receptors. The LTD4-induced increases in [Ca+2]i were dependent on extracellular calcium and diminished by lanthanum, but not affected by nifedipine nor associated with changes in membrane potential, as measured with the fluorescent probe 3,3'-dipentyloxacarbocyanine. Thus, the increase in [Ca+2]i in HL-60 cells, which is coupled to an increase in adherence, appears to involve LTD4 receptor-specific and voltage-independent calcium channels in the plasma membrane.