- Macrophage deletion of Noc4l triggers endosomal TLR4/TRIF signal and leads to insulin resistance.
Macrophage deletion of Noc4l triggers endosomal TLR4/TRIF signal and leads to insulin resistance.
Nature communications (2021-10-23)
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, Xiangdong Li
PMID34675215
RÉSUMÉ
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.
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Sigma-Aldrich
Collagénase from Clostridium histolyticum, suitable for release of physiologically active rat epididymal adipocytes, Type II, 0.5-5.0 FALGPA units/mg solid, ≥125 CDU/mg solid