Mitofusin 2 in Macrophages Links Mitochondrial ROS Production, Cytokine Release, Phagocytosis, Autophagy, and Bactericidal Activity.
apoptotic bodies
inflammation
lipopolysaccharide (LPS)
macrophages
mitochondria
mitofusin
phagocytosis
protein degradation
reactive oxygen species (ROS)
septic shock
Journal
Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691
Informations de publication
Date de publication:
25 08 2020
25 08 2020
Historique:
received:
27
07
2018
revised:
02
07
2020
accepted:
05
08
2020
entrez:
27
8
2020
pubmed:
28
8
2020
medline:
3
6
2021
Statut:
ppublish
Résumé
Mitofusin 2 (Mfn2) plays a major role in mitochondrial fusion and in the maintenance of mitochondria-endoplasmic reticulum contact sites. Given that macrophages play a major role in inflammation, we studied the contribution of Mfn2 to the activity of these cells. Pro-inflammatory stimuli such as lipopolysaccharide (LPS) induced Mfn2 expression. The use of the Mfn2 and Mfn1 myeloid-conditional knockout (KO) mouse models reveals that Mfn2 but not Mfn1 is required for the adaptation of mitochondrial respiration to stress conditions and for the production of reactive oxygen species (ROS) upon pro-inflammatory activation. Mfn2 deficiency specifically impairs the production of pro-inflammatory cytokines and nitric oxide. In addition, the lack of Mfn2 but not Mfn1 is associated with dysfunctional autophagy, apoptosis, phagocytosis, and antigen processing. Mfn2
Identifiants
pubmed: 32846136
pii: S2211-1247(20)31064-0
doi: 10.1016/j.celrep.2020.108079
pii:
doi:
Substances chimiques
Reactive Oxygen Species
0
GTP Phosphohydrolases
EC 3.6.1.-
Mfn2 protein, mouse
EC 3.6.1.-
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
108079Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Interests The authors declare no competing interests.