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首页> 外文期刊>Journal of Cellular Physiology >Evidence that IL-6-type cytokine signaling in cardiomyocytes is inhibited by oxidative stress: parthenolide targets JAK1 activation by generating ROS.
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Evidence that IL-6-type cytokine signaling in cardiomyocytes is inhibited by oxidative stress: parthenolide targets JAK1 activation by generating ROS.

机译：证据表明IL-6-type细胞因子信号抑制了心肌细胞氧化应激:parthenolide目标JAK1激活产生活性氧。

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摘要

Parthenolide, an anti-inflammatory compound, was reported to inhibit signal transducer and activator of transcription 3 (STAT3) activation by the interleukin (IL)-6-type cytokines by an undefined process, which was the focus of our study. Here we report that parthenolide reduced both basal and leukemia inhibitory factor (LIF)-induced STAT3 tyrosine 705 (Y705) phosphorylation in cardiomyocytes in a dose-dependent manner, but stimulated the MAP kinase signaling pathways. Activation of Janus kinase 1 (JAK1) tyrosine kinase was markedly reduced by parthenolide. Pretreatment with parthenolide inhibited JAK1-mediated phosphorylation of the LIF receptor subunits LIF receptor (LIFR) alpha and glycoprotein 130 (gp130), and reduced the LIF-induced increase in JAK1 association with both components. In addition, we documented that parthenolide, over the same concentration range, does not have a direct inhibitory effect on JAK1 autophosphorylation. However, we observed that parthenolide increased intracellular reactive oxygen species (ROS). Pretreatment with the antioxidant, N-acetyl-L-cysteine, completely suppressed the effect of parthenolide on JAK1 and STAT3. From these results, we conclude ROS generation in cardiomyocytes blocks STAT3 signaling of the IL-6-type cytokines by targeting JAK1. The finding that signaling by the IL-6-type cytokine may be redox-sensitive defines a novel mechanism of regulation that has implications for exploiting their therapeutic potential.
机译：Parthenolide、消炎药据报道,抑制信号传感器和激活的转录3 (STAT3)激活细胞因子白介素(IL)型的未定义的过程,这是我们的重点研究。基底和白血病抑制因子705(生活)全身STAT3酪氨酸(Y705)在心肌细胞磷酸化剂量依赖性的方式,但刺激了地图激酶信号通路。激酶1 (JAK1)酪氨酸激酶是明显的减少parthenolide。parthenolide抑制JAK1-mediated磷酸化的生活受体亚基的生活受体(LIFR)α和糖蛋白130(gp130),减少LIF-induced增加JAK1协会与组件。另外,我们记录parthenolide,结束了相同的浓度范围,没有JAK1直接抑制作用自身磷酸化。parthenolide增加细胞内活性氧物种(ROS)。氧化剂,N-acetyl-L-cysteine,完全抑制parthenolide JAK1和的影响STAT3。一代STAT3在心肌细胞块针对IL-6-type细胞因子的信号JAK1。细胞因子可能redox-sensitive定义了一个小说监管的影响机制利用他们的治疗潜力。

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