Glucose metabolism controls monocyte homeostasis and migration but has no impact on atherosclerosis development in mice

Alexandre Gallerand (), Bastien Dolfi, Marion I. Stunault, Zakariya Caillot, Alexia Castiglione, Axelle Strazzulla, Chuqiao Chen, Gyu Seong Heo, Hannah Luehmann, Flora Batoul, Nathalie Vaillant, Adélie Dumont, Thomas Pilot, Johanna Merlin, Fairouz N. Zair, Jerome Gilleron, Adeline Bertola, Peter Carmeliet, Jesse W. Williams, Rafael J. Arguello, David Masson, David Dombrowicz, Laurent Yvan-Charvet, Denis Doyen, Arvand Haschemi, Yongjian Liu, Rodolphe R. Guinamard and Stoyan Ivanov ()
Additional contact information
Alexandre Gallerand: CNRS
Bastien Dolfi: CNRS
Marion I. Stunault: INSERM, C3M
Zakariya Caillot: CNRS
Alexia Castiglione: CNRS
Axelle Strazzulla: CNRS
Chuqiao Chen: Medical University of Vienna
Gyu Seong Heo: Washington University School of Medicine
Hannah Luehmann: Washington University School of Medicine
Flora Batoul: INSERM, C3M
Nathalie Vaillant: INSERM, C3M
Adélie Dumont: INSERM, C3M
Thomas Pilot: LNC UMR1231
Johanna Merlin: INSERM, C3M
Fairouz N. Zair: CNRS
Jerome Gilleron: INSERM, C3M
Adeline Bertola: CNRS
Peter Carmeliet: KU Leuven
Jesse W. Williams: University of Minnesota Medical School
Rafael J. Arguello: Centre d’Immunologie de Marseille-Luminy
David Masson: LNC UMR1231
David Dombrowicz: Institut Pasteur de Lille, U1011-EGID
Laurent Yvan-Charvet: INSERM, C3M
Denis Doyen: CNRS
Arvand Haschemi: Medical University of Vienna
Yongjian Liu: Washington University School of Medicine
Rodolphe R. Guinamard: CNRS
Stoyan Ivanov: CNRS

Nature Communications, 2024, vol. 15, issue 1, 1-16

Abstract: Abstract Monocytes directly contribute to atherosclerosis development by their recruitment to plaques in which they differentiate into macrophages. In the present study, we ask how modulating monocyte glucose metabolism could affect their homeostasis and their impact on atherosclerosis. Here we investigate how circulating metabolites control monocyte behavior in blood, bone marrow and peripheral tissues of mice. We find that serum glucose concentrations correlate with monocyte numbers. In diet-restricted mice, monocytes fail to metabolically reprogram from glycolysis to fatty acid oxidation, leading to reduced monocyte numbers in the blood. Mechanistically, Glut1-dependent glucose metabolism helps maintain CD115 membrane expression on monocytes and their progenitors, and regulates monocyte migratory capacity by modulating CCR2 expression. Results from genetic models and pharmacological inhibitors further depict the relative contribution of different metabolic pathways to the regulation of CD115 and CCR2 expression. Meanwhile, Glut1 inhibition does not impact atherosclerotic plaque development in mouse models despite dramatically reducing blood monocyte numbers, potentially due to the remaining monocytes having increased migratory capacity. Together, these data emphasize the role of glucose uptake and intracellular glucose metabolism in controlling monocyte homeostasis and functions.

Date: 2024
References: View references in EconPapers View complete reference list from CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-024-53267-5 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-53267-5

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-024-53267-5

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().