Macrophage deletion of Noc4l triggers endosomal TLR4/TRIF signal and leads to insulin resistance.
Journal
Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555
Informations de publication
Date de publication:
21 10 2021
21 10 2021
Historique:
received:
26
04
2019
accepted:
19
08
2021
entrez:
22
10
2021
pubmed:
23
10
2021
medline:
15
12
2021
Statut:
epublish
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.
Identifiants
pubmed: 34675215
doi: 10.1038/s41467-021-26408-3
pii: 10.1038/s41467-021-26408-3
pmc: PMC8531303
doi:
Substances chimiques
Adaptor Proteins, Vesicular Transport
0
TICAM-1 protein, mouse
0
Toll-Like Receptor 4
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
6121Informations de copyright
© 2021. The Author(s).
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