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首页> 外文期刊>Cellular Signalling >Inhibition by Rho-kinase and protein kinase C of myosin phosphatase is involved in thrombin-induced shape change of megakaryocytic leukemia cell line UT-7/TPO
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Inhibition by Rho-kinase and protein kinase C of myosin phosphatase is involved in thrombin-induced shape change of megakaryocytic leukemia cell line UT-7/TPO

机译：Rho激酶和蛋白激酶C对肌球蛋白磷酸酶的抑制作用与凝血酶诱导的巨核细胞白血病细胞系UT-7 / TPO的形状改变有关

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摘要

Thrombin induced a shape change of UT-7/TPO, a thrombopoietin-dependent human megakaryocytic cell line. Expression of myosin light chain (MLC) kinase was negligible in UT-7/TPO cells, while Rho-kinase and protein kinase C (PKC) were detected. Thrombin stimulated both monophosphorylation at Ser19 and diphosphorylation at Thr18 and Ser19 of 20 kDa MLC, as well as phosphorylation of myosin-binding subunit (MBS) and PKC-potentiated inhibitory phosphoprotein of myosin phosphatase (CPI). The Rho-kinase inhibitor Y-27632 [(+)-(R)-trans-(1-aminoethyl)-N-(4-phynidyl) cyclohexane-carboxamide dihydrochloride, monohydrade] strongly inhibited thrombin-induced shape change, MBS phosphorylation, and mono- and diphosphorylation of MLC. The PKC inhibitor GF109203X (2-[1-(3-dimethylaminopropyl)-1H-indol-3-yl]-3-(1H-indol-3-yl)-maleimide) partially inhibited thrombin-induced shape change and MLC diphosphorylation even at the concentration that completely inhibited thrombin-induced CPI phosphorylation. In shape-changed UT-7/TPO cells induced by thrombin, phosphorylated MBS and CPI were colocalized with diphosphorylated MLC at pseudopods, whereas monophosphorylated MLC was mainly located in the cortical region. The accumulation of diphosphorylated MLC was blocked by preincubation with either Y-27632 or GF109203X. These results suggest that Rho-kinase is responsible for the induction of MLC phosphorylation in thrombin-induced shape change of UT-7/TPO cells and that myosin phosphatase inactivation through Rho-kinase-MBS and PKC-CPI pathways could be necessary for enhancement of MLC diphosphorylation which promote the pseudopod formation. (C) 2004 Elsevier Inc. All rights reserved.
机译：凝血酶诱导UT-7 / TPO的形状变化，这是血小板生成素依赖性的人类巨核细胞系。在UT-7 / TPO细胞中，肌球蛋白轻链（MLC）激酶的表达可忽略不计，而检测到Rho激酶和蛋白激酶C（PKC）。凝血酶刺激20kDa MLC的Ser19处的单磷酸化和Thr18和Ser19处的二磷酸化，以及肌球蛋白结合亚基（MBS）和PKC增强的肌球蛋白磷酸酶（CPI）抑制性磷酸化蛋白的磷酸化。 Rho激酶抑制剂Y-27632 [（+）-（R）-反式-（1-氨基乙基）-N-（4-菲啶基）环己烷甲酰胺二盐酸盐，一水合物]强烈抑制凝血酶诱导的形状变化，MBS磷酸化，以及MLC的单磷酸化和二磷酸化PKC抑制剂GF109203X（2- [1-（3-二甲基氨基丙基）-1H-吲哚-3-基] -3-（1H-吲哚-3-基）-马来酰亚胺）部分抑制凝血酶诱导的形状变化和MLC二磷酸化完全抑制凝血酶诱导的CPI磷酸化的浓度。在凝血酶诱导的UT-7 / TPO形状改变的细胞中，磷酸化的MBS和CPI与二磷酸化的MLC共定位于假足，而单磷酸化的MLC主要位于皮层区域。通过与Y-27632或GF109203X的预孵育来阻止二磷酸化MLC的积累。这些结果表明，Rho激酶负责诱导凝血酶诱导的UT-7 / TPO细胞形状变化中的MLC磷酸化，并且通过Rho激酶-MBS和PKC-CPI途径失活的肌球蛋白磷酸酶可能是增强MHC磷酸化所必需的。 MLC二磷酸化促进伪足形成。 （C）2004 Elsevier Inc.保留所有权利。

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