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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Role of the actin cytoskeleton in angiotensin II signaling in human vascular smooth muscle cells.
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Role of the actin cytoskeleton in angiotensin II signaling in human vascular smooth muscle cells.

机译：肌动蛋白细胞骨架在人血管平滑肌细胞中血管紧张素II信号传导中的作用。

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Angiotensin II (Ang II) regulates vascular smooth muscle cell (VSMC) function by activating signaling cascades that promote vasoconstriction, growth, and inflammation. Subcellular mechanisms coordinating these processes are unclear. In the present study, we questioned the role of the actin cytoskeleton in Ang II mediated signaling through mitogen-activated protein (MAP) kinases and reactive oxygen species (ROS) in VSMCs. Human VSMCs were studied. Cells were exposed to Ang II (10-7 mol/L) in the absence and presence of cytochalasin B (10-6 mol/L, 60 min), which disrupts the actin cytoskeleton. Phosphorylation of p38MAP kinase, JNK, and ERK1/2 was assessed by immuno blotting. ROS generation was measured using the fluoroprobe chloromethyl-2',7'-dichlorodihydrofluorescein diacetate (4 micromol/L). Interaction between the cytoskeleton and NADPH oxidase was determined by evaluating the presence of p47phox in the Triton X-100 insoluble membrane fraction. Ang II significantly increased phosphorylation of p38MAP kinase, JNK, and ERK1/2 (two- to threefold above control, p < 0.05). Cytochalasin B pretreatment attenuated p38MAP kinase and JNK effects (p < 0.05) without altering ERK1/2 phosphorylation. ROS formation, which was increased in Ang II stimulated cells, was significantly reduced by cytochalasin B (p < 0.01). p47phox, critically involved in NADPH oxidase activation, colocalized with the actin cytoskeleton in Ang II stimulated cells. Our data demonstrate that Ang II mediated ROS formation and activation of p38MAP kinase and JNK, but not ERK1/2, involves the actin cytoskeleton in VSMCs. In addition, Ang II promotes interaction between actin and p47phox. These data indicate that the cytoskeleton is involved in differential MAP kinase signaling and ROS generation by Ang II in VSMCs. Together, these studies suggest that the cytoskeleton may be a central point of crosstalk in growth- and redox-signaling pathways by Ang II, which may be important in the regulation of VSMC function.
机译：血管紧张素II（Ang II）通过激活促进血管收缩，生长和炎症的信号级联反应来调节血管平滑肌细胞（VSMC）的功能。协调这些过程的亚细胞机制尚不清楚。在本研究中，我们质疑肌动蛋白的细胞骨架在血管紧张素Ⅱ中通过促分裂原活化蛋白（MAP）激酶和活性氧（ROS）介导的Ang II介导的信号传导中的作用。研究了人类VSMC。在不存在和存在细胞松弛素B（10-6 mol / L，60分钟）的情况下，将细胞暴露于Ang II（10-7 mol / L），这会破坏肌动蛋白的细胞骨架。通过免疫印迹评估p38MAP激酶，JNK和ERK1 / 2的磷酸化。使用氟乙酸-2'，7'-二氯二氢荧光素二乙酸酯（4 micromol / L）测量ROS的生成。通过评估Triton X-100不溶膜组分中p47phox的存在，可以确定细胞骨架与NADPH氧化酶之间的相互作用。 Ang II显着增加p38MAP激酶，JNK和ERK1 / 2的磷酸化（比对照高2到3倍，p <0.05）。细胞松弛素B预处理可减弱p38MAP激酶和JNK的作用（p <0.05），而不会改变ERK1 / 2磷酸化。松弛素B可以显着减少Ang II刺激的细胞中ROS的形成（p <0.01）。 p47phox关键参与NADPH氧化酶的活化，在Ang II刺激的细胞中与肌动蛋白细胞骨架共定位。我们的数据表明，Ang II介导的ROS的形成和p38MAP激酶和JNK的激活，而不是ERK1 / 2，涉及VSMC中的肌动蛋白细胞骨架。另外，Ang II促进肌动蛋白和p47phox之间的相互作用。这些数据表明，细胞骨架与VSMC中Ang II引起的差异MAP激酶信号传导和ROS产生有关。总之，这些研究表明，细胞骨架可能是Ang II在生长和氧化还原信号通路中串扰的中心点，这可能对VSMC功能的调节很重要。

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