Kunitama M, Shimizu R, Yamada M, Kato T, Miyazaki H, Okada K, Miura Y, Komatsu N
Department of Medicine, Jichi Medical School, Tochigi-ken, Japan.
Biochem Biophys Res Commun. 1997 Feb 13;231(2):290-4. doi: 10.1006/bbrc.1996.5969.
Thrombopoietin (TPO) is the major regulator of the proliferation and differentiation of megakaryocyte precursors through interaction with its receptor encoded by the c-mpl protooncogene. We established the human TPO-dependent leukemia cell line, UT-7/TPO (Blood 87, 4552, 1996). In these cells, TPO activated protein kinase C (PKC) in a time dependent manner. Subsequently, the c-myc gene was transiently induced to a maximal level 60-90 minutes after TPO exposure. In addition, we found that stimulating UT-7/TPO cells with TPO rapidly induces the significant accumulation of inositol 1, 4, 5-trisphosphate (Ins-P3), leading to the mobilization of calcium from intracellular stores. Taken together, the activation of PKC and subsequent c-myc gene induction are involved in the TPO-induced cellular response(s), presumably through the activation of PLC.
血小板生成素（TPO）是巨核细胞前体增殖和分化的主要调节因子，它通过与c-mpl原癌基因编码的受体相互作用来发挥作用。我们建立了依赖人TPO的白血病细胞系UT-7/TPO（《血液》第87卷，第4552页，1996年）。在这些细胞中，TPO以时间依赖性方式激活蛋白激酶C（PKC）。随后，c-myc基因在TPO作用60 - 90分钟后被短暂诱导至最高水平。此外，我们发现用TPO刺激UT-7/TPO细胞会迅速诱导肌醇1,4,5-三磷酸（Ins-P3）的显著积累，导致细胞内钙库中的钙动员。综上所述，PKC的激活以及随后的c-myc基因诱导可能通过磷脂酶C（PLC）的激活参与了TPO诱导的细胞反应。
