Hato T, Sumida M, Yasukawa M, Watanabe A, Okuda H, Kobayashi Y
Department of Internal Medicine, School of Medicine, Ehime University, Japan.
Blood. 1990 Mar 1;75(5):1087-91.
We found that a monoclonal antibody (MoAb) to CD9 antigen, PMA2, induced a rise in cytosolic free calcium concentration ([Ca2+]i) in fura-2-loaded platelets, and we examined whether this response was due to direct action of PMA2 on CD9 antigen. The rise in [Ca2+]i was dependent on the PMA2 concentration, irrespective of the presence or absence of extracellular Ca2+. The role of secreted adenosine diphosphate (ADP) and thromboxane in the [Ca2+]i response to PMA2 was studied using creatine phosphate/creatine phosphokinase (CP/CPK) and aspirin. Combined treatment with CP/CPK and aspirin abolished the rise in [Ca2+]i, although either CP/CPK or aspirin alone produced only partial inhibition. Inhibition of adenosine triphosphate (ATP) secretion and thromboxane B2 synthesis by an MoAb to the glycoprotein IIb-IIIa complex, PMA1, resulted in little [Ca2+]i response to PMA2. In contrast, thrombasthenic platelets, in which ATP secretion and thromboxane B2 synthesis were normal, showed a normal [Ca2+]i response. When PMA2 was added to CD9+ mononuclear cells, no rise in [Ca2+]i was observed. Thus, we conclude that binding of monoclonal immunoglobulin G molecules to the CD9 antigen raises [Ca2+]i through the effect of secreted ADP and thromboxane on platelets, and that CD9 antigen is not directly involved in induction of Ca2+ influx and mobilization.
我们发现，一种针对CD9抗原的单克隆抗体（MoAb）PMA2可使负载fura-2的血小板胞质游离钙浓度（[Ca2+]i）升高，我们研究了这种反应是否是由于PMA2对CD9抗原的直接作用所致。[Ca2+]i的升高取决于PMA2的浓度，与细胞外Ca2+的存在与否无关。使用磷酸肌酸/磷酸肌酸激酶（CP/CPK）和阿司匹林研究了分泌的二磷酸腺苷（ADP）和血栓素在[Ca2+]i对PMA2反应中的作用。CP/CPK和阿司匹林联合处理可消除[Ca2+]i的升高，尽管单独使用CP/CPK或阿司匹林仅产生部分抑制作用。一种针对糖蛋白IIb-IIIa复合物的MoAb PMA1抑制三磷酸腺苷（ATP）分泌和血栓素B2合成，导致对PMA2的[Ca2+]i反应很小。相反，ATP分泌和血栓素B2合成正常的血小板无力症血小板对PMA2显示出正常的[Ca2+]i反应。当将PMA2添加到CD9+单核细胞中时，未观察到[Ca2+]i升高。因此，我们得出结论，单克隆免疫球蛋白G分子与CD9抗原的结合通过分泌的ADP和血栓素对血小板的作用提高了[Ca2+]i，并且CD9抗原不直接参与Ca2+内流和动员的诱导。
