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首页> 外文期刊>Cell biology international. >Lipopolysaccharide increases IL-6 secretion via activation of the ERK1/2 signaling pathway to up-regulate RANKL gene expression in MLO-Y4 cells
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Lipopolysaccharide increases IL-6 secretion via activation of the ERK1/2 signaling pathway to up-regulate RANKL gene expression in MLO-Y4 cells

机译：脂多糖通过激活ERK1 / 2信号传导途径以上调MLO-Y4细胞中的RANCHL基因表达来增加IL-6分泌

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摘要

Lipopolysaccharide (LPS) plays an important role in bone resorption, which involves numerous cytokines through various signaling pathways. RANKL and interleukin (IL)-6 are two important cytokines that are involved in bone remodeling. The aim of this study was to evaluate the effect of LPS on RANKL and IL-6 gene expression, the relationship of RANKL and IL-6, and the role of extracellular signal-regulated kinases 1/2 (ERK1/2) on IL-6 secretion induced by LPS in MLO-Y4 cells. The cells were stimulated by LPS at different concentrations (1, 10, 100, 500, and 1000ng/mL) for different durations (0.5, 1, 2, 4, and 8h and 0.5, 1, 1.5, 2, and 4h), and the mRNA expressions of RANKL and IL-6 were determined by PCR. In the presence of 100ng/mL LPS at different time points (0.5, 1, 1.5, 2, and 4h), IL-6 secretion and ERK1/2 phosphorylation in the cells were determined by ELISA and western blotting, respectively. STAT3 phosphorylation in cells simulated by 100ng/mL LPS at different time points (0.5, 1, 2, 4, and 8h) was assessed by western blotting. We found that LPS significantly up-regulated RANKL expression and activated the ERK1/2 pathway to induce IL-6 mRNA expression and protein synthesis in MLO-Y4 cells. However, the increased IL-6 was blocked by pre-treatment of MLO-Y4 cells with the ERK1/2 inhibitor U0126 (10 mu M), and the enhanced RANKL was blocked by the STAT3 inhibitor S3I-201 (100 mu M). Our results indicate that LPS up-regulates osteocyte expression of RANKL and IL-6, and the increased RANKL is associated with the up-regulation of IL-6, which involves the ERK1/2 pathway.
机译：脂多糖（Lipopolysaccharide，LPS）在骨吸收中起着重要作用，它通过多种信号通路参与多种细胞因子。RANKL和白细胞介素-6是参与骨重建的两种重要细胞因子。本研究旨在评估LPS对RANKL和IL-6基因表达的影响，RANKL和IL-6之间的关系，以及细胞外信号调节激酶1/2（ERK1/2）在LPS诱导MLO-Y4细胞分泌IL-6中的作用。用不同浓度（1,10,100,500和1000ng/mL）的LPS刺激细胞，持续不同时间（0.5,1,2,4和8h以及0.5,1,1.5,2和4h），并通过PCR检测RANKL和IL-6的mRNA表达。在不同时间点（0.5、1、1.5、2和4h）存在100ng/mL LPS的情况下，通过ELISA和western blotting分别测定细胞中的IL-6分泌和ERK1/2磷酸化。通过western印迹法评估在不同时间点（0.5、1、2、4和8h）用100ng/mL LPS模拟的细胞中STAT3磷酸化。我们发现，在MLO-Y4细胞中，LPS显著上调RANKL表达，激活ERK1/2通路，诱导IL-6mRNA表达和蛋白质合成。然而，增加的IL-6被ERK1/2抑制剂U0126（10μM）预处理的MLO-Y4细胞阻断，而增强的RANKL被STAT3抑制剂S3I-201（100μM）阻断。我们的结果表明，LPS上调骨细胞RANKL和IL-6的表达，RANKL的增加与IL-6的上调有关，后者涉及ERK1/2途径。

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  • 来源
    《Cell biology international.》 |2017年第1期|共9页
  • 作者

    Yu Ke; Ma Yuanyuan; Li Xianxian; Wu Xiangnan; Liu Wenjia; Li Xiaoyu; Shen Jiefei; Wang Hang;

  • 作者单位

    Sichuan Univ State Key Lab Oral Dis Chengdu 610041 Peoples R China;

    Sun Yat Sen Univ Guanghua Sch Stomatol Hosp Stomatol Guangzhou 510055 Guangdong Peoples R China;

    Sichuan Acad Med Sci Chengdu 610041 Peoples R China;

    Sichuan Univ State Key Lab Oral Dis Chengdu 610041 Peoples R China;

    Sichuan Univ State Key Lab Oral Dis Chengdu 610041 Peoples R China;

    Sichuan Univ State Key Lab Oral Dis Chengdu 610041 Peoples R China;

    Sichuan Univ State Key Lab Oral Dis Chengdu 610041 Peoples R China;

    Sichuan Univ State Key Lab Oral Dis Chengdu 610041 Peoples R China;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;
  • 关键词

    ERK1; 2; interleukin-6; lipopolysaccharide; osteocyte; RANKL;

    机译：ERK1;2;白细胞介素-6;脂多糖;骨细胞;RANKL;

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