The mitochondrial succinate dehydrogenase complex controls the STAT3-IL-10 pathway in inflammatory macrophages.

Détails

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Etat: Public
Version: Final published version
Licence: CC BY-NC-ND 4.0
ID Serval
serval:BIB_D70FF9529DAB
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
The mitochondrial succinate dehydrogenase complex controls the STAT3-IL-10 pathway in inflammatory macrophages.
Périodique
iScience
Auteur⸱e⸱s
Gobelli D., Serrano-Lorenzo P., Esteban-Amo M.J., Serna J., Pérez-García M.T., Orduña A., Jourdain A.A., Martín-Casanueva M.Á., Á de la Fuente M., Simarro M.
ISSN
2589-0042 (Electronic)
ISSN-L
2589-0042
Statut éditorial
Publié
Date de publication
18/08/2023
Peer-reviewed
Oui
Volume
26
Numéro
8
Pages
107473
Langue
anglais
Notes
Publication types: Journal Article
Publication Status: epublish
Résumé
The functions of macrophages are tightly regulated by their metabolic state. However, the role of the mitochondrial electron transport chain (ETC) in macrophage functions remains understudied. Here, we provide evidence that the succinate dehydrogenase (SDH)/complex II (CII) is required for respiration and plays a role in controlling effector responses in macrophages. We find that the absence of the catalytic subunits Sdha and Sdhb in macrophages impairs their ability to effectively stabilize HIF-1α and produce the pro-inflammatory cytokine IL-1β in response to LPS stimulation. We also arrive at the novel result that both subunits are essential for the LPS-driven production of IL-10, a potent negative feedback regulator of the macrophage inflammatory response. This phenomenon is explained by the fact that the absence of Sdha and Sdhb leads to the inhibition of Stat3 tyrosine phosphorylation, caused partially by the excessive accumulation of mitochondrial reactive oxygen species (mitoROS) in the knockout cells.
Mots-clé
Biological sciences, Cell biology, Immunology, Molecular biology
Pubmed
Web of science
Open Access
Oui
Création de la notice
21/08/2023 8:22
Dernière modification de la notice
25/01/2024 8:45
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