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Macrophage deletion of Noc4l triggers endosomal TLR4/TRIF signal and leads to insulin resistance

Author

Listed:
  • Yongli Qin

    (State Key Laboratory of Agrobiotechnology, College of Biological Sciences, China Agricultural University)

  • Lina Jia

    (State Key Laboratory of Agrobiotechnology, College of Biological Sciences, China Agricultural University)

  • Huijiao Liu

    (State Key Laboratory of Agrobiotechnology, College of Biological Sciences, China Agricultural University)

  • Wenqiang Ma

    (State Key Laboratory of Agrobiotechnology, College of Biological Sciences, China Agricultural University)

  • Xinmin Ren

    (State Key Laboratory of Agrobiotechnology, College of Biological Sciences, China Agricultural University)

  • Haifeng Li

    (State Key Laboratory of Agrobiotechnology, College of Biological Sciences, China Agricultural University)

  • Yuanwu Liu

    (State Key Laboratory of Agrobiotechnology, College of Biological Sciences, China Agricultural University)

  • Haiwen Li

    (Agricultural Research Station, College of Agriculture, Virginia State University)

  • Shuoqian Ma

    (State Key Laboratory of Agrobiotechnology, College of Biological Sciences, China Agricultural University)

  • Mei Liu

    (Chinese PLA General Hospital)

  • Pingping Li

    (Academy of Medical Sciences & Peking Union, Medical College)

  • Jinghua Yan

    (CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences)

  • Jiyan Zhang

    (Institute of Basic Medical Sciences)

  • Yangdong Guo

    (State Key Laboratory of the Agro-Biotechnology, College of Horticultural Science, China Agricultural University)

  • Hua You

    (Affiliated Cancer Hospital & Institute of Guangzhou Medical University)

  • Yan Guo

    (State Key Laboratory of Agrobiotechnology, College of Biological Sciences, China Agricultural University)

  • Nafis A. Rahman

    (Institute of Biomedicine, University of Turku
    Medical University of Bialystok)

  • Sławomir Wołczyński

    (Medical University of Bialystok)

  • Adam Kretowski

    (Medical University of Bialystok)

  • Dangsheng Li

    (Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences)

  • Xiru Li

    (Chinese PLA General Hospital)

  • Fazheng Ren

    (China Agricultural University)

  • Xiangdong Li

    (State Key Laboratory of Agrobiotechnology, College of Biological Sciences, China Agricultural University
    Medical University of Bialystok)

Abstract

In obesity, macrophages drive a low-grade systemic inflammation (LSI) and insulin resistance (IR). The ribosome biosynthesis protein NOC4 (NOC4) mediates 40 S ribosomal subunits synthesis in yeast. Hereby, we reported an unexpected location and function of NOC4L, which was preferentially expressed in human and mouse macrophages. NOC4L was decreased in both obese human and mice. The macrophage-specific deletion of Noc4l in mice displayed IR and LSI. Conversely, Noc4l overexpression by lentivirus treatment and transgenic mouse model improved glucose metabolism in mice. Importantly, we found that Noc4l can interact with TLR4 to inhibit its endocytosis and block the TRIF pathway, thereafter ameliorated LSI and IR in mice.

Suggested Citation

  • Yongli Qin & Lina Jia & Huijiao Liu & Wenqiang Ma & Xinmin Ren & Haifeng Li & Yuanwu Liu & Haiwen Li & Shuoqian Ma & Mei Liu & Pingping Li & Jinghua Yan & Jiyan Zhang & Yangdong Guo & Hua You & Yan Gu, 2021. "Macrophage deletion of Noc4l triggers endosomal TLR4/TRIF signal and leads to insulin resistance," Nature Communications, Nature, vol. 12(1), pages 1-18, December.
    • Handle: RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-26408-3
    DOI: 10.1038/s41467-021-26408-3
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