Oda Masaaki, Kurasawa Yasuhiro, Todokoro Kazuo, Nagata Yuka
Laboratory of Molecular Cell Science, RIKEN (The Institute of Physical and Chemical Research), 2-1 Hirosawa, Wako, Saitama 351-0198, Japan.
Genes Cells. 2003 Jan;8(1):9-15. doi: 10.1046/j.1365-2443.2003.00610.x.
We previously reported that the expressions of two CXC chemokines, neutrophil activating peptide-2 (NAP-2) and platelet factor-4 (PF-4), were induced by megakaryocyte-specific cytokine thrombopoietin (TPO) in mouse bone marrow megakaryocytes. The roles of these chemokines on megakaryocyte maturation/differentiation processes, including polyploidization and proplatelet formation (PPF) remain unresolved.
NAP-2 and PF-4 suppressed the PPF of mature megakaryocytes freshly prepared from mouse bone marrow as well as that of the megakaryocyte progenitors, c-Kit+CD41+ cells, isolated from mouse bone marrow and cultured with TPO. NAP-2 and PF-4 inhibited polyploidization of c-Kit+CD41+ cells in the presence of TPO, and also inhibited the proliferation of c-Kit+CD41+ cells.
NAP-2 and PF-4 produced by TPO stimulation in megakaryocytes suppress megakaryocyte maturation and proliferation as a feedback control.
我们之前报道过，两种CXC趋化因子，即中性粒细胞激活肽-2（NAP-2）和血小板因子-4（PF-4），在小鼠骨髓巨核细胞中由巨核细胞特异性细胞因子血小板生成素（TPO）诱导表达。这些趋化因子在巨核细胞成熟/分化过程中的作用，包括多倍体化和前血小板形成（PPF），仍未明确。
NAP-2和PF-4抑制了从小鼠骨髓新鲜制备的成熟巨核细胞以及从小鼠骨髓分离并与TPO一起培养的巨核细胞祖细胞c-Kit+CD41+细胞的PPF。NAP-2和PF-4在TPO存在的情况下抑制了c-Kit+CD41+细胞的多倍体化，并且还抑制了c-Kit+CD41+细胞的增殖。
巨核细胞中TPO刺激产生的NAP-2和PF-4作为反馈控制抑制巨核细胞的成熟和增殖。
