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首页> 外文期刊>Journal of Cellular Physiology >Extracellular ATP causes of loss of L-selectin from human lymphocytes via occupancy of P2Z purinocepters.
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Extracellular ATP causes of loss of L-selectin from human lymphocytes via occupancy of P2Z purinocepters.

机译：细胞外ATP L-selectin损失的原因从人类淋巴细胞通过P2Z的入住率purinocepters。

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摘要

Lymphocytes from normal subjects or patients with chronic lymphocytic leukemia are known to possess receptors for extracellular ATP termed P2Z purinoceptors whose physiological role is undefined. Addition of extracellular ATP (50-500 microM) to both normal and leukemic lymphocytes caused loss of binding of monoclonal antibodies to L-selectin (CD62L) on the cell surface. UTP, ADP, and adenosine (all at 500 microM) had no effect on L-selectin expression. Several features of the ATP-induced loss of L selectin indicate that this effect is mediated by lymphocyte P2Z purinoceptors. First the loss was attenuated in isotonic NaCl medium compared to 150 mM KCl medium. Second the loss of L-selectin was immediately halted by addition of Mg2+ ions in molar excess of ATP. The most potent nucleotide causing L-selectin loss was benzoylbenzoic ATP (> 10 microM) which is also the most potent agonist for the P2Z purinoceptor. Finally preincubation of lymphocytes with oxidized ATP, an irreversible inhibitor of P2Z purinoceptors, also inhibited ATP induced loss of L-selectin. Extracellular ATP is known to open an ion channel associated with the P2Z purinoceptor on B-lymphocytes which allows influx of Ca2+. However, ATP-induced loss of L-selectin did not require extracellular Ca2+. Moreover addition of the calcium ionophore, ionomycin, had minimal effect on L-selectin expression. Staurosporine (500 nM), an inhibitor of protein kinase C, inhibited only 10% of ATP induced loss of L-selectin but completely inhibited the loss of L-selectin caused by 50 nM PMA. Thus extracellular ATP interacts with lymphocyte P2Z purinoceptors which leads to shedding of L-selectin via a pathway which requires neither Ca2+ influx nor activation of protein kinase C. ATP may have a physiological role in the loss of L-selectin which occurs during the interactions of lymphocytes with other cells.
机译：淋巴细胞从正常受试者或患者慢性淋巴细胞白血病具有受体细胞外ATP称为P2Zpurinoceptors的生理作用未定义的。microM)正常和白血病淋巴细胞绑定的单克隆抗体引起的L-selectin (CD62L)在细胞表面。ADP和腺苷(所有500 microM)没有影响L-selectin表达式。L selectin ATP-induced损失的指示这种效果是由淋巴细胞P2Zpurinoceptors。等渗氯化钠介质相比,150毫米氯化钾媒介。立即停止Mg2 +离子的添加摩尔过剩的ATP。导致L-selectin亏损benzoylbenzoic ATP (>10 microM)也是最强有力的兴奋剂为P2Z purinoceptor。淋巴细胞的氧化ATP,不可逆转抑制剂的P2Z purinoceptors,也抑制ATP诱导L-selectin的损失。众所周知,离子通道与开放的P2Z purinoceptor淋巴细胞上允许Ca2 +的涌入。L-selectin不需要细胞外钙离子。此外添加钙离子载体,对L-selectin ionomycin,最小的影响表达式。蛋白激酶C、抑制ATP的只有10%诱导L-selectin但完全丧失抑制造成的损失L-selectin 50 nMPMA。淋巴细胞P2Z purinoceptors导致脱落的L-selectin通过这一途径需要Ca2 +涌入和激活蛋白激酶c ATP可能有生理L-selectin发生的损失在淋巴细胞的相互作用与其他细胞。

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