Effects of microparticles on monocyte-derived procoagulant activity provoked via SP : NK1R pathway

P物质（SP）通过白细胞中的神经激肽-1受体（NK 1 R）增强全血凝固，但这种现象的确切机制仍有待建立。因此，评价了与组织因子相关的微粒对通过SP：NK 1 R途径引起的单核细胞衍生的促凝血活性的影响。CC趋化因子配体5（CCL 5）增加从单核细胞释放的微粒。SP增强CCL 5依赖的微粒从这些细胞的释放。在单核细胞中不组成型表达的全长NK 1 R的强制表达也增强了微粒从这些细胞中的释放。

Substance-P(SP) enhances whole blood coagulation through neurokinin-1 receptors(NK1R) in leukocytes while the precise mechanisms of this phenomenon remains to be established. Thus the effects of microparticles associated with tissue factor on monocyte-derived procoagulant activity provoked via SP : NK1R pathway were evaluated. CC chemokine ligand 5(CCL5) increased microparticles released from monocytes. SP enhanced CCL5-dependent release of microparticles from these cells. Forced expression of the full-length NK1R that is not constitutively expressed in monocytes also enhanced the release of microparticles from these cells.