Analysis of mechanism of human megakaryocyte maturation

对人巨核细胞成熟的机制进行了研究.研究Evi-1对巨核细胞的作用。Evi-1 mRNA在CMK和Meg-J两个巨核细胞白血病细胞系中表达。然而，在TPA（12-0-tetradecanoyl phorbol-13-acetate）、IL-3（interleukin-3）、IL-6或IL-11刺激后，Evi-1 mRNA的表达没有增加。结论：1. CMK细胞表达myb mRNA，而加入myb寡核苷酸不能抑制CMK细胞的增殖，提示myb对CMK细胞的增殖没有作用.当Meg-J细胞在蛋白激酶C抑制剂K252 a存在下培养时，倍性显著向更高的值转移。该检测系统可用于研究巨核细胞的多倍化机制.酪氨酸激酶抑制剂Herbimycin A可阻断TPA对CMK细胞CD 41表达的促进作用，表明TPA诱导的CD 41表达是由酪氨酸激酶介导的。

The mechanism of maturation of human megakaryocytic cells has been investigated.1. The role of Evi-1 on megakaryocytic cells was investigated. Evi-1 m-RNA was expressed in two megakaryoblastic leukemia cell lines, CMK and Meg-J.However Evi-1 m-RNA expression did not increase after stimulation by TPA (12-0-tetradecanoyl phorbol-13-acetate), IL-3 (interleukin-3), IL-6 or IL-11. Myb m-RNA was expressed in CMK cells however, addition of oligonucleotide of myb to CMK cells chould not suppress the proliferation, suggesting that myb has no role for the proliferation of CMK cells.2. When Meg-J cells were cultured in the presence of K252a, a protein kinase C inhibitor, the ploidy was dramatically shifted toward higher values. This assay system may be useful for studying the mechnism of polyploidization of megakaryocytic cells.3. Enhancement of CD41 expression of CMK cells by TPA was ablogated by Herbimycin A,a tyrosine kinase inhibitor, indicating that TPA-induced CD41 expression was mediated by tyrosine kinases.