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

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 Guo, Nafis A. Rahman, Sławomir Wołczyński, Adam Kretowski, Dangsheng Li, Xiru Li, Fazheng Ren and Xiangdong Li ()
Additional contact information
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
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

Nature Communications, 2021, vol. 12, issue 1, 1-18

Abstract: 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.

Date: 2021
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DOI: 10.1038/s41467-021-26408-3

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