ADP-induced血小板活化的分子基础。二世。P2Y1受体介导ADP-induced血小板胞内钙动员和形状变化。
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金J,丹尼尔·杰Kunapuli SP
ADP-induced血小板活化的分子基础。二世。P2Y1受体介导ADP-induced血小板胞内钙动员和形状变化。
J生物化学杂志。1998年1月23日,273 (4):2030 - 4。
- PubMed ID
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9442040 (在PubMed]
- 文摘
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ADP是一个重要的血小板受体激动剂导致形状变化平滑铁饼状的形状针状的球体和血小板聚集。然而,ADP-induced血小板激活的分子机制尚未阐明。早些时候我们演示了两个截然不同的ADP血小板受体的存在,一个耦合的磷脂酶C, P2TPLC,和其他抑制腺苷酸环化酶,P2TAC (Daniel j . L。Dangelmaier C。金,J。,阿什比B。,史密斯,j·B。,Kunapuli s p(1998)生物。化学。273年,2024 - 2029),除了先前描述P2X1受体。在这里,我们报告的克隆cDNA克隆编码P2Y1受体从人类血小板cDNA图书馆与放射性标记的同源性筛选P2Y1-P2Y6受体的互补。ADP或2 -甲基(含硫的)-ADP-induced胞内钙增加抑制了P2Y1针对受体拮抗剂,腺苷三磷酸的5 ' -phosphosulfate (A3P5PS)、腺苷三磷酸的5 '磷酸(A3P5P)和腺苷2的磷酸5 '磷酸(A2P5P)浓度的方式,但不是由陆军研究实验室的66096或α,beta-MeATP。A3P5PS、A3P5P A2P5P也抑制了aspirinated的形状变化引起的血小板10 microM ADP或3 microM 2 -甲基-(硫代的)浓度的方式ADP,完全抑制发生在300 microM。 On the other hand ARL 66096 (100 nM), a potent P2TAC antagonist and alpha, beta-methylene-ATP (40 microM), a P2X1 receptor agonist, had no effect on ADP-induced platelet shape change. On the contrary, ADP-induced inhibition of adenylyl cyclase was blocked by ARL 66096, but not by alpha, beta-MeATP or the P2Y1 receptor-specific antagonists, A3P5PS, A3P5P, or A2P5P. These results demonstrate the role of the P2Y1 receptor in ADP-induced platelet shape change and calcium mobilization and support the idea that several P2 receptors are involved in the regulation of different aspects of platelet stimulus-response coupling.