Interaction between lymphocytes and platelets in the synthesis of prostacyclin.
Interaction between lymphocytes and platelets in the synthesis of prostacyclin.
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DOI：
10.1172/jci112995
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发表时间：
1987-06
期刊：
影响因子：
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通讯作者：
K. Wu;A. Papp;C. Manner;E. Hall
中科院分区：
文献类型：
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作者：
K. Wu;A. Papp;C. Manner;E. Hall
为了验证前列环素（PGI 2）是通过血小板和淋巴细胞之间的生化相互作用形成的假设，我们用高效液相色谱法（HPLC）和放射免疫测定法（RIA）测定了类花生酸。当[14 C]花生四烯酸（[14 C]AA）加入混合细胞制剂中时，观察到一个明显的6-酮-前列腺素F1 α（6 KPGF 1 α）峰，用1-苄基咪唑（1-BI）预处理血小板可增加该峰。用植物血凝素（PHA）或离子载体A23187刺激时，[14 C]AA预标记的淋巴细胞不能形成6 KPGF 1 α。当预先标记的血小板与阿司匹林处理的淋巴细胞一起悬浮，并用离子载体、凝血酶或胶原蛋白刺激时，检测到6 KPGF 1 α峰，并通过1-BI增强。通过RIA定量HPLC纯化级分中的6 KPGF 1 α含量支持这些结果。将前列腺素H2（PGH 2）直接加入淋巴细胞导致6 KPGF 1 α的产生。淋巴细胞对血小板聚集和释放有抑制作用，且呈剂量相关性。我们的结论是，淋巴细胞具有PGI 2合酶活性，能够将血小板衍生的PGH 2转化为PGI 2。形成的PGI 2足以抑制血小板功能。
To test the hypothesis that prostacyclin (PGI2) is formed via a biochemical interaction between platelets and lymphocytes, we measured eicosanoids by high performance liquid chromatography (HPLC) and radioimmunoassay (RIA). A distinct 6-keto-prostaglandin F1 alpha (6KPGF1 alpha) peak was noted when [14C]arachidonic acid ([14C]AA) was added to the mixed cell preparations which was increased by pretreating platelets with 1-benzylimidazole (1-BI). Lymphocytes prelabeled with [14C]AA failed to form 6KPGF1 alpha when stimulated with phytohemagglutinin (PHA) or ionophore A23187. When the prelabeled platelets were suspended together with aspirin-treated lymphocytes and stimulated with ionophore, thrombin, or collagen, a 6KPGF1 alpha peak was detected and enhanced by 1-BI. These results were supported by quantifying the 6KPGF1 alpha content in the HPLC-purified fraction by RIA. Adding prostaglandin H2 (PGH2) directly to lymphocytes led to 6KPGF1 alpha production. Platelet aggregation and release were inhibited by lymphocytes in a dose-related manner. We conclude that lymphocytes possess PGI2 synthase activity which is capable of converting platelet-derived PGH2 into PGI2. PGI2 formed is sufficient to inhibit platelet function.