Mitofusin 2 Deficiency Causes Pro-Inflammatory Effects in Human Primary Macrophages.
Cytokines
/ metabolism
Endoplasmic Reticulum
/ metabolism
Endoplasmic Reticulum Stress
/ physiology
GTP Phosphohydrolases
/ deficiency
Humans
Inflammation
/ metabolism
Macrophages
/ metabolism
Mitochondria
/ metabolism
Mitochondrial Proteins
/ deficiency
Mitogen-Activated Protein Kinases
/ metabolism
Reactive Oxygen Species
/ metabolism
Signal Transduction
/ physiology
endoplasmic reticulum
inflammation
macrophages
mitochondria
mitochondrial dynamics
zymosan
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2021
2021
Historique:
received:
11
06
2021
accepted:
28
07
2021
entrez:
30
8
2021
pubmed:
31
8
2021
medline:
21
12
2021
Statut:
epublish
Résumé
Mitofusin 2 (MFN2) is a mitochondrial outer membrane GTPase, which modulates mitochondrial fusion and affects the interaction between endoplasmic reticulum and mitochondria. Here, we explored how MFN2 influences mitochondrial functions and inflammatory responses towards zymosan in primary human macrophages. A knockdown of MFN2 by small interfering RNA decreased mitochondrial respiration without attenuating mitochondrial membrane potential and reduced interactions between endoplasmic reticulum and mitochondria. A MFN2 deficiency potentiated zymosan-elicited inflammatory responses of human primary macrophages, such as expression and secretion of pro-inflammatory cytokines interleukin-1β, -6, -8 and tumor necrosis factor α, as well as induction of cyclooxygenase 2 and prostaglandin E
Identifiants
pubmed: 34456930
doi: 10.3389/fimmu.2021.723683
pmc: PMC8397414
doi:
Substances chimiques
Cytokines
0
Mitochondrial Proteins
0
Reactive Oxygen Species
0
Mitogen-Activated Protein Kinases
EC 2.7.11.24
GTP Phosphohydrolases
EC 3.6.1.-
MFN2 protein, human
EC 3.6.1.-
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
723683Informations de copyright
Copyright © 2021 Khodzhaeva, Schreiber, Geisslinger, Brandes, Brüne and Namgaladze.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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