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Macrophage deletion of Noc4l triggers endosomal TLR4/TRIF signal and leads to insulin resistance
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 i...
| Autores principales: | , , , , , , , , , , , , , , , , , , , , , , |
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| Formato: | Online Artículo Texto |
| Lenguaje: | English |
| Publicado: |
Nature Publishing Group UK
2021
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| Materias: | |
| Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8531303/ https://www.ncbi.nlm.nih.gov/pubmed/34675215 http://dx.doi.org/10.1038/s41467-021-26408-3 |
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| author | Qin, Yongli Jia, Lina Liu, Huijiao Ma, Wenqiang Ren, Xinmin Li, Haifeng Liu, Yuanwu Li, Haiwen Ma, Shuoqian Liu, Mei Li, Pingping Yan, Jinghua Zhang, Jiyan Guo, Yangdong You, Hua Guo, Yan Rahman, Nafis A. Wołczyński, Sławomir Kretowski, Adam Li, Dangsheng Li, Xiru Ren, Fazheng Li, Xiangdong |
| author_facet | Qin, Yongli Jia, Lina Liu, Huijiao Ma, Wenqiang Ren, Xinmin Li, Haifeng Liu, Yuanwu Li, Haiwen Ma, Shuoqian Liu, Mei Li, Pingping Yan, Jinghua Zhang, Jiyan Guo, Yangdong You, Hua Guo, Yan Rahman, Nafis A. Wołczyński, Sławomir Kretowski, Adam Li, Dangsheng Li, Xiru Ren, Fazheng Li, Xiangdong |
| author_sort | Qin, Yongli |
| collection | PubMed |
| description | 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. |
| format | Online Article Text |
| id | pubmed-8531303 |
| institution | National Center for Biotechnology Information |
| language | English |
| publishDate | 2021 |
| publisher | Nature Publishing Group UK |
| record_format | MEDLINE/PubMed |
| spelling | pubmed-85313032021-10-22 Macrophage deletion of Noc4l triggers endosomal TLR4/TRIF signal and leads to insulin resistance Qin, Yongli Jia, Lina Liu, Huijiao Ma, Wenqiang Ren, Xinmin Li, Haifeng Liu, Yuanwu Li, Haiwen Ma, Shuoqian Liu, Mei Li, Pingping Yan, Jinghua Zhang, Jiyan Guo, Yangdong You, Hua Guo, Yan Rahman, Nafis A. Wołczyński, Sławomir Kretowski, Adam Li, Dangsheng Li, Xiru Ren, Fazheng Li, Xiangdong Nat Commun Article 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. Nature Publishing Group UK 2021-10-21 /pmc/articles/PMC8531303/ /pubmed/34675215 http://dx.doi.org/10.1038/s41467-021-26408-3 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
| spellingShingle | Article Qin, Yongli Jia, Lina Liu, Huijiao Ma, Wenqiang Ren, Xinmin Li, Haifeng Liu, Yuanwu Li, Haiwen Ma, Shuoqian Liu, Mei Li, Pingping Yan, Jinghua Zhang, Jiyan Guo, Yangdong You, Hua Guo, Yan Rahman, Nafis A. Wołczyński, Sławomir Kretowski, Adam Li, Dangsheng Li, Xiru Ren, Fazheng Li, Xiangdong Macrophage deletion of Noc4l triggers endosomal TLR4/TRIF signal and leads to insulin resistance |
| title | Macrophage deletion of Noc4l triggers endosomal TLR4/TRIF signal and leads to insulin resistance |
| title_full | Macrophage deletion of Noc4l triggers endosomal TLR4/TRIF signal and leads to insulin resistance |
| title_fullStr | Macrophage deletion of Noc4l triggers endosomal TLR4/TRIF signal and leads to insulin resistance |
| title_full_unstemmed | Macrophage deletion of Noc4l triggers endosomal TLR4/TRIF signal and leads to insulin resistance |
| title_short | Macrophage deletion of Noc4l triggers endosomal TLR4/TRIF signal and leads to insulin resistance |
| title_sort | macrophage deletion of noc4l triggers endosomal tlr4/trif signal and leads to insulin resistance |
| topic | Article |
| url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8531303/ https://www.ncbi.nlm.nih.gov/pubmed/34675215 http://dx.doi.org/10.1038/s41467-021-26408-3 |
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