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首页> 外文期刊>Journal of Cellular Physiology >Up-regulation of Ca2+ influx mediated by store-operated channels in HL60 cells induced to differentiate by 1 alpha,25-dihydroxyvitamin D3.
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Up-regulation of Ca2+ influx mediated by store-operated channels in HL60 cells induced to differentiate by 1 alpha,25-dihydroxyvitamin D3.

机译：老年病的Ca2 +由涌入门店渠道诱导HL60细胞区分1α,25-dihydroxyvitamin D3。

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摘要

The physiologically active form of vitamin D, 1 alpha,25-dihydroxyvitamin D3 (1,25D3), induces promyelocytic HL60 cells to differentiate towards monocyte-like cells. During this differentiation increased cytosolic calcium (Cai2+) and expression of surface receptors for chemotactic factors "prime" the cell for the activation of monocyte functions and the triggering of the respiratory burst pathway. We examined whether the Ca2+ influx mediated by store-operated channels (SOC) contributed to the increased Cai2+ following exposure of HL60 cells to 10(-7) M 1,25D3. Cells treated with 1,25D3 for 72 hr demonstrated a rapid transient rise in Cai2+ followed by a second, phasic, increase in Cai2+ in response to the purinergic agonist ATP. This second Cai2+ transient was blocked by Ni2+, SKF 96365, or withdrawal of extracellular Ca2+. In cells suspended in Ca(2+)-free medium, peak changes (delta) in [Ca2+]i elicited by ATP-induced Ca2+ mobilization occurred with similar EC50 values in differentiated and vehicle (EtOH)-treated cells; however, peak [Ca2+]i was reduced by 55% in 1,25D3-treated cells. Decreased Ca2+ mobilization was associated with a 25-35% reduction in intracellular Ca2+ stores (determined with ionomycin). 1,25D3-treated cells exposed to ATP or thapsigargin (Tg) in Ca(2+)-free medium for 3 min with subsequent addition of 1 mM Ca2+ exhibited a respective 80% or 120% stimulation in peak [Ca2+]i compared to EtOH-treated cells. Enhanced Ca2+ influx mediated by SOC was also seen in these cells as an increase in the rate of Mn2+ entry after exposure to ATP or Tg. At 96 hr after addition of 1,25D3, when differentiated phenotype was established, basal Ca2+i and Ca2+ entry mediated by SOC returned to control values, but Ca2+ store size remained reduced. Up-regulation of Ca2+ influx via the SOC pathway during 1,25D3-induced differentiation may contribute to the functional properties of the maturing monocyte, or to the resetting of molecular programs responsible for the changing phenotype.
机译：生理活性形式的维生素D, 1α,25-dihydroxyvitamin D3 (1,25 D3),诱发早幼粒细胞HL60细胞分化monocyte-like细胞。胞质钙(裁+)和增加趋化现象的表面受体的表达因素激活的细胞“'”单核细胞的触发功能呼吸途径。钙离子流入由门店通道(SOC)导致了增加裁+曝光后HL60细胞10(7)米1,25 d3。演示了一个快速瞬态裁+紧随其后的第二个阶段,提高裁+为了应对purinergic兴奋剂ATP。第二个裁+瞬态被Ni2 +, SKF96365年,或细胞外钙离子的撤退。细胞悬浮在Ca(2 +)无介质,峰值变化(δ)[Ca2 +]我了ATP-induced Ca2 +动员发生在分化和车辆类似EC50值(EtOH)治疗细胞;减少55%的1,25 d3-treated细胞。Ca2 +动员与25 - 35%降低细胞内钙离子的商店与ionomycin(决定)。暴露在ATP或thapsigargin (Tg)Ca(2 +)无介质与后续3分钟增加1毫米Ca2 +展出各自的80%或120%相比,峰[Ca2 +]我刺激EtOH-treated细胞。通过SOC也看到在这些细胞增加的速率Mn2 +曝光后入境ATP或Tg。当分化表型,成立基底Ca2 +我和Ca2 +条目由SOC返回值来控制,但Ca2 +存储大小仍减少。通过SOC通路在1,25 d3-induced分化可能导致的功能成熟的单核细胞的属性,或重置的分子程序负责表型的变化。

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