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首页> 外文期刊>Journal of Cellular Physiology >Cytoplasmic elongation and rupture in megakaryoblastic leukemia cells via activation of adhesion and motility by staurosporine on fibronectin-bound substratum.
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Cytoplasmic elongation and rupture in megakaryoblastic leukemia cells via activation of adhesion and motility by staurosporine on fibronectin-bound substratum.

机译：细胞质伸长和破裂通过激活megakaryoblastic白血病细胞附着力和运动性staurosporinefibronectin-bound下层。

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Human megakaryoblastic leukemia Meg-01 cells were attached to fibronectin (FN)-coated substratum, on which remarkable spreading and cytoplasmic elongation was induced by treatment with a protein kinase inhibitor, staurosporine (stp). This effect was inhibited by RGDS and was also not seen on FN-lacking substratum. The extended cytoplasm had swollen terminals and nodes, which contained GpIIb and beta-thromboglobulin, occasionally included alpha granules, and tended to form particles (2-5 microm) after rupture of the narrowed cytoplasm. Among other protein kinase modulators tested, only K252a promoted the elongation, while calphostin, herbimycin, TPA, and calyculin suppressed it. The cells began to migrate soon after addition of stp, with attachment to the substratum held at some sites during the migration. This tethered movement seemed to cause the cytoplasmic elongation and the rupture into particles. The elongation was retarded by pretreating the cells with cytochalasin A and Clostridium C3 toxin but not with demecolcine. Actin microfilaments in the stp-treated Meg-01 cells accumulated in the filopodia and periphery of the extended cytoplasm, in which vinculin was colocalized as adhesion plaques. The microtubules were longitudinally oriented through the cytoplasmic extension and showed no ring profile in the nodes and particles. Thus, stp in the presence of FN appears to stimulate reorganization of actin-based cytoskeleton and formation of focal contacts in Meg-01 cells. This leads to the activation of cell adhesion and motility, and then cytoplasmic elongation and rupture into particles.
机译：人类Meg-01 megakaryoblastic白血病细胞附加到纤连蛋白(FN)涂布下层,非凡的传播和细胞质伸长是治疗引起的蛋白激酶抑制剂,staurosporine (stp)。这种效应被RGDS抑制,也未见对FN-lacking下层。细胞质肿胀的终端节点,包含GpIIb beta-thromboglobulin,偶尔包括α颗粒和倾向形成颗粒破裂后(2 - 5 microm)缩小细胞质。激酶调节器进行测试,只有K252a促进了伸长,而calphostin herbimycin TPA,和calyculin压制它。迁移的stp后不久,附件在一些网站的基础在迁移。似乎导致细胞质伸长和破裂成粒子。推迟通过预处理细胞细胞松弛素和C3梭状芽胞杆菌毒素而不是秋水仙胺。stp-treated Meg-01细胞中积累丝状伪足和外围扩展细胞质,vinculin与作为粘附斑。纵向的细胞质扩展和没有环配置文件的节点和粒子。似乎刺激重组actin-based细胞骨架和焦的形成在Meg-01细胞接触。激活细胞粘附和能动性然后细胞质伸长断裂粒子。

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