K562 leukemia cells express P2T (adenosine diphosphate) purinergic receptors.
K562 leukemia cells express P2T (adenosine diphosphate) purinergic receptors.
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K562 白血病细胞表达 P2T（二磷酸腺苷）嘌呤能受体。
DOI：
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发表时间：
1992
影响因子：
3.5
通讯作者：
F. Sistare
中科院分区：
文献类型：
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作者：
A. Murgo;F. Sistare
ADP的P2 T嘌呤能受体以前仅在血小板中发现。我们研究了ADP对Fura-2负载的K562白血病细胞（一种具有巨核细胞分化潜能的细胞系）细胞内游离钙（[Ca++]i）浓度的影响。ADP引起[Ca++]i的快速和短暂增加，其在5至10秒内达到峰值。该反应的EC 50为0.4 μ M。增加的钙的主要部分是由于细胞内储存的动员，因为在细胞外钙不存在的情况下，对ADP的反应仅部分降低。暴露于ADP使K562细胞对该核苷酸的额外施用脱敏。用蛋白激酶C激活剂佛波醇12-肉豆蔻酸酯13-乙酸酯预处理K562细胞完全阻断对ADP的反应。佛波醇12-肉豆蔻酸酯13-乙酸酯的这种作用被蛋白激酶C抑制剂staurosporine阻止，但staurosporine不影响重复ADP暴露后脱敏的进展。ATP不增加K562细胞内[Ca++]i，但可拮抗ADP对细胞内[Ca++] i的作用。我们认为K562细胞中ADP的P2 T受体是巨核细胞分化的早期标志。此外，这种永生化的有核细胞系可能是一个有用的模型，以破译参与ADP反应的信号转导途径。
The P2T purinergic receptor for ADP has previously been found only in platelets. We investigated the effect of ADP on the concentration of intracellular free calcium ([Ca++]i) in fura-2-loaded K562 leukemia cells, a cell line with the potential for megakaryocytic differentiation. ADP causes a rapid and transient increase in [Ca++]i, which peaks within 5 to 10 sec. The EC50 for this response is 0.4 microM. A major portion of the increased calcium is due to mobilization of intracellular stores because the response to ADP is only partially reduced in the absence of extracellular calcium. Exposure to ADP desensitizes K562 cells to additional administrations of this nucleotide. Pretreatment of K562 cells with the protein kinase C activator phorbol 12-myristate 13-acetate completely blocks the response to ADP. This effect of phorbol 12-myristate 13-acetate is prevented by the protein kinase C inhibitor staurosporine, but staurosporine does not affect the progression of desensitization after repeated ADP exposures. ATP does not increase [Ca++]i in K562 cells, but antagonizes the response to ADP. We propose that the P2T receptor for ADP in K562 cells is an early marker for megakaryocytic differentiation. Furthermore, this immortalized nucleated cell line may be a useful model to decipher the signal transduction pathways involved in the ADP response.