Macrophage beta2-adrenergic receptor is dispensable for the adipose tissue inflammation and function.
Adipocytes
/ metabolism
Adipose Tissue, White
/ metabolism
Animals
Atherosclerosis
/ complications
Bone Marrow Transplantation
/ methods
Cells, Cultured
Diet, High-Fat
/ adverse effects
Diet, Western
/ adverse effects
Disease Models, Animal
Female
Insulin Resistance
/ genetics
Macrophages
/ metabolism
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Obesity
/ complications
Panniculitis
/ genetics
Phenotype
Receptors, Adrenergic, beta-2
/ genetics
Signal Transduction
/ genetics
Sympathetic Nervous System
/ metabolism
Atherosclerosis
Immunometabolism
Neuroimmune
Norepinephrine
Sympathetic
adrb2
Journal
Molecular metabolism
ISSN: 2212-8778
Titre abrégé: Mol Metab
Pays: Germany
ID NLM: 101605730
Informations de publication
Date de publication:
06 2021
06 2021
Historique:
received:
01
02
2021
revised:
18
03
2021
accepted:
20
03
2021
pubmed:
29
3
2021
medline:
21
1
2022
entrez:
28
3
2021
Statut:
ppublish
Résumé
Neuroimmune interactions between the sympathetic nervous system (SNS) and macrophages are required for the homeostasis of multiple tissues, including the adipose tissue. It has been proposed that the SNS maintains adipose tissue macrophages (ATMs) in an anti-inflammatory state via direct norepinephrine (NE) signaling to macrophages. This study aimed to investigate the physiological importance of this paradigm by utilizing a mouse model in which the adrenergic signaling from the SNS to macrophages, but not to other adipose tissue cells, was disrupted. We generated a macrophage-specific B2AR knockout mouse (Adrb2 We demonstrated that SNS-associated ATMs have a transcriptional profile indicative of activated beta-2 adrenergic receptor (B2AR), the main adrenergic receptor isoform in myeloid cells. However, Adrb2 Overall, our data suggest that the SNS does not directly modulate the phenotype of adipose tissue macrophages in either lean mice or mouse models of cardiometabolic disease. Instead, sympathetic nerve activity exerts an indirect effect on adipose tissue macrophages through the modulation of adipocyte function.
Identifiants
pubmed: 33774223
pii: S2212-8778(21)00064-8
doi: 10.1016/j.molmet.2021.101220
pmc: PMC8086137
pii:
doi:
Substances chimiques
ADRB2 protein, mouse
0
Receptors, Adrenergic, beta-2
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
101220Subventions
Organisme : Medical Research Council
ID : MC_UU_00014/2
Pays : United Kingdom
Organisme : British Heart Foundation
ID : RG/12/13/29853
Pays : United Kingdom
Organisme : Department of Health
Pays : United Kingdom
Organisme : British Heart Foundation
ID : CH/10/001/27642
Pays : United Kingdom
Organisme : Medical Research Council
ID : G0802051
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 100574/Z/12/Z
Pays : United Kingdom
Organisme : Medical Research Council
ID : G0400192
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_G0802535
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_UU_12012/5
Pays : United Kingdom
Organisme : British Heart Foundation
ID : RCAG969
Pays : United Kingdom
Organisme : British Heart Foundation
ID : RG/18/7/33636
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_UU_12012/2
Pays : United Kingdom
Organisme : British Heart Foundation
ID : PG/15/99/31865
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 102354/Z/13/Z
Pays : United Kingdom
Informations de copyright
Copyright © 2021 The Author(s). Published by Elsevier GmbH.. All rights reserved.