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首页> 外文期刊>Cell biology international. >ER stress differentially affects pro‐inflammatory changes induced by mitochondrial dysfunction in the human monocytic leukemia cell line, THP‐1
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ER stress differentially affects pro‐inflammatory changes induced by mitochondrial dysfunction in the human monocytic leukemia cell line, THP‐1

机译：ER应激差异地影响人类单核细胞白血病细胞系中线粒体功能障碍诱导的促炎变化，THP-1

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摘要

Abstract The functional and physical interaction between mitochondria and the endoplasmic reticulum (ER) has been the subject of intense study. To test the effect of this interaction on macrophage inflammatory activation, the human macrophage‐like monocytic leukemia cell line THP‐1 was treated with oligomycin, rotenone, or sodium azide, which induce mitochondrial dysfunction (MD) by blocking the electron transport chain (ETC). MD induced by these agents triggered activation of various sensors and markers of ER stress. This linkage affected macrophage function since LPS‐induced expression of IL‐23 was enhanced by the MD inducers, and this enhancing effect was abolished by inhibition of pancreatic endoplasmic reticulum kinase (PERK) activity. This MD‐mediated ER stress may be universal since it was observed in human embryonic kidney HEK293 cells and colon cancer SW480 cells. On the other hand, MD regulated LPS‐induced activation of the AKT/GSK3β/β‐catenin pathway in a manner not affected by inhibition of PERK or inositol‐requiring enzyme 1α (IRE1α) activities. These results indicate that the occurrence of MD can lead to ER stress and these two events, separately or in combination, can affect various cellular processes.
机译：摘要线粒体与内质网（ER）之间的功能和物理相互作用是激烈研究的主题。为了测试这种相互作用对巨噬细胞炎症激活的影响，用寡霉素，旋转酮或叠氮化钠处理人巨噬细胞样单核细胞细胞系THP-1，通过阻挡电子传输链（ETC）诱导线粒体功能障碍（MD）。 ）。由这些药剂诱导的MD触发了各种传感器的激活和ER应力的标记。这种联动影响巨噬细胞功能，因为MD诱导仪增强了LPS诱导的IL-23的表达，并且通过抑制胰腺内质网激酶（PERK）活性来消除这种增强效果。这种MD介导的ER应力可能是普遍的，因为它在人胚胎肾HEK293细胞和结肠癌SW480细胞中观察到。另一方面，MD调节LPS诱导的AKT /GSK3β/β-连环蛋白途径以不受抑制Perk或肌醇的酶1α（IRE1α）活性影响的方式。这些结果表明，MD的发生可以导致ER应激，并且这些事件分别或组合可以影响各种细胞过程。

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  • 来源
    《Cell biology international.》 |2019年第3期|共10页
  • 作者

    Heo Jae‐Nyoung; Kim Dong‐Yeon; Lim Su‐Geun; Lee Kiboo; Suk Kyoungho; Lee Won‐Ha;

  • 作者单位

    School of Life Sciences BK21 Plus KNU Creative BioResearch GroupKyungpook National UniversityDaegu;

    School of Life Sciences BK21 Plus KNU Creative BioResearch GroupKyungpook National UniversityDaegu;

    School of Life Sciences BK21 Plus KNU Creative BioResearch GroupKyungpook National UniversityDaegu;

    School of Life Sciences BK21 Plus KNU Creative BioResearch GroupKyungpook National UniversityDaegu;

    Department of Pharmacology Brain Science &

    Engineering InstituteBK21 Plus KNU Biomedical;

    School of Life Sciences BK21 Plus KNU Creative BioResearch GroupKyungpook National UniversityDaegu;

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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

    ER stress; inflammation; macrophage; mitochondrial dysfunction;

    机译：ER应激;炎症;巨噬细胞;线粒体功能障碍;

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