Analysis of the molecular mechanism regulated during megakaryopoiesis and platelet function

巨核细胞(MKs)在一种谱系特异的细胞因子--血小板生成素(TPO)的控制下从造血干细胞分化而来。成熟的最后阶段的特征是从称为原血小板的细长细胞质过程的末端释放血小板。然而，单核细胞产生的调节原血小板形成和血小板活化的机制还不完全清楚。在本研究中，野生型(WT)和CD226基因敲除(KO)、Calastatin KO或P38A+/-MKs和血小板之间的原血小板形成和包括CD62P和PS暴露的血小板功能是不同的。这些结果提示CD226、calain-calastatin和p38MAPK参与了血小板原的形成和功能。

Megakaryocytes (MKs) differentiate from hematopoietic stem cells under the control of a lineage-specific cytokine, thrombopoietin (TPO). Final stage of the maturation is characterized by platelet release from the ends of long thin cytoplasmic processes called proplatelet. However, the mechanism for regulating proplatelet formation and platelet activation produced from MKs have not been completely understood. In this study, proplatelet formation and platelet function including CD62P and PS exposure were different between wild-type (WT) and CD226 knockout (KO) or calpastatin KO or p38a +/- MKs and platelets. These results suggest that CD226, calpain-calpastatin and p38 MAPK are involved in proplatelet formation and platelet function.