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Original Research

Disruption of Glut1 in Hematopoietic Stem Cells Prevents Myelopoiesis and Enhanced Glucose Flux in Atheromatous Plaques of ApoE-/- Mice

Vincent Sarrazy, Manon Viaud, Marit Westerterp, Stoyan Ivanov, Sophie Giorgetti-Peraldi, Rodolphe Guinamard, Emmanuel L Gautier, Edward B Thorp, Darryl C De Vivo, Laurent Yvan-Charvet
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https://doi.org/10.1161/CIRCRESAHA.115.307599
Circulation Research. 2016;CIRCRESAHA.115.307599
Originally published February 29, 2016
Vincent Sarrazy
Matrix Dynamics Group, Faculty of Dentistry, University of Toronto
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Manon Viaud
Bâtiment Universitaire ARCHIMED, INSERM U1065
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Marit Westerterp
Molecular Medicine, Columbia University
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Stoyan Ivanov
Méditerranéen de Médecine Moléculaire (C3M), INSERM U1065
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Sophie Giorgetti-Peraldi
Méditerranéen de Médecine Moléculaire (C3M), INSERM U1065
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Rodolphe Guinamard
Bâtiment Universitaire ARCHIMED, INSERM U1065
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Emmanuel L Gautier
UMRS 1166, INSERM
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Edward B Thorp
Pathology, Northwestern University
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Darryl C De Vivo
Neurology, Columbia University
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Laurent Yvan-Charvet
Bâtiment Universitaire ARCHIMED, INSERM U1065
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  • For correspondence: yvancharvet@unice.fr
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Abstract

Rationale: Inflamed atherosclerotic plaques can be visualized by non-invasive PET-CT imaging with 18FDG, a glucose analog but the underlying mechanisms are poorly understood.

Objective: Here, we directly investigated the role of Glut1-mediated glucose uptake in ApoE-/- mouse model of atherosclerosis.

Methods and Results: We first show that the enhanced glycolytic flux in atheromatous plaques of ApoE-/- mice was associated with the enhanced metabolic activity of hematopoietic stem and multi-potential progenitors (HSPCs) and higher Glut1 expression in these cells. Mechanistically, the regulation of Glut1 in ApoE-/- HSPCs was not due to alterations in hypoxia-inducible factor 1α (HIF1α) signaling or the oxygenation status of the bone marrow but was the consequence of the activation of the common β subunit of the granulocyte macrophage colony-stimulating factor/interleukin-3 receptor driving glycolytic substrate utilization by mitochondria. By transplanting BM from WT, Glut1+/-, ApoE-/- and ApoE-/-Glut1+/- mice into hypercholesterolemic ApoE deficient mice, we found that Glut1 deficiency reversed ApoE-/- HSPC proliferation and expansion, which prevented the myelopoiesis and accelerated atherosclerosis of ApoE-/- mice transplanted with ApoE-/- BM and resulted in reduced glucose uptake in the spleen and aortic arch of these mice.

Conclusions: We identified that Glut1 connects the enhanced glucose uptake in atheromatous plaques of ApoE-/- mice with their myelopoiesis through regulation of HSPC maintenance and myelomonocytic fate and suggest Glut1 as potential drug target for atherosclerosis.

  • cell cycling
  • myeloid commitment
  • Glut1
  • atherosclerosis
  • bone marrow
  • cholesterol
  • hematopoietic stem cells
  • glucose glycolysis
  • Received September 10, 2015.
  • Revision received February 25, 2016.
  • Accepted February 26, 2016.
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    Disruption of Glut1 in Hematopoietic Stem Cells Prevents Myelopoiesis and Enhanced Glucose Flux in Atheromatous Plaques of ApoE-/- Mice
    Vincent Sarrazy, Manon Viaud, Marit Westerterp, Stoyan Ivanov, Sophie Giorgetti-Peraldi, Rodolphe Guinamard, Emmanuel L Gautier, Edward B Thorp, Darryl C De Vivo and Laurent Yvan-Charvet
    Circulation Research. 2016;CIRCRESAHA.115.307599, originally published February 29, 2016
    https://doi.org/10.1161/CIRCRESAHA.115.307599

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    Disruption of Glut1 in Hematopoietic Stem Cells Prevents Myelopoiesis and Enhanced Glucose Flux in Atheromatous Plaques of ApoE-/- Mice
    Vincent Sarrazy, Manon Viaud, Marit Westerterp, Stoyan Ivanov, Sophie Giorgetti-Peraldi, Rodolphe Guinamard, Emmanuel L Gautier, Edward B Thorp, Darryl C De Vivo and Laurent Yvan-Charvet
    Circulation Research. 2016;CIRCRESAHA.115.307599, originally published February 29, 2016
    https://doi.org/10.1161/CIRCRESAHA.115.307599
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