Analysis of the molecular mechanism regulated during megakaryopoiesis and platelet function

巨核细胞（mk）在谱系特异性细胞因子——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点是血小板从称为前血小板的长而薄的细胞质过程的末端释放出来。然而，mk对血小板前形成和血小板活化的调控机制尚不完全清楚。在这项研究中，野生型（WT）和CD226敲除（KO）或calpastatin KO或p38a +/- mk与血小板之间的血小板形成和血小板功能，包括CD62P和PS暴露是不同的。这些结果提示CD226、calpain-calpastatin和p38 MAPK参与血小板形成和血小板功能。

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.