Article
Deletion of Macrophage Vitamin D Receptor
Promotes Insulin Resistance and Monocyte
Cholesterol Transport to Accelerate Atherosclerosis
in Mice
Graphical Abstract Authors
Jisu Oh, Amy E. Riek, ...,
Richard E. Ostlund, Jr.,
Carlos Bernal-Mizrachi
Correspondence
******@
In Brief
Identifying environmental conditions
affecting chronic inflammation is
essential to preventing cardiometabolic
disorders. Oh et al. demonstrate that
myeloid-specific Vdr deletion is sufficient
to induce insulin resistance and
accelerate atherosclerosis in mice.
Furthermore, M2 monocyte transport of
cholesterol into the vessel wall is
described as a low-density lipoprotein
(LDL)-independent pathway for
atherosclerosis.
Highlights
d Myeloid VDR deletion induces hepatic macrophage
deposition and gluconeogenesis
d Myeloid VDR deletion enables M2 monocytes to transport
cholesterol into plaques
d Impaired VDR-SERCA2b interaction results in macrophage
ER stress and foam cells
d Bone marrow transplant of VDR into KODMAC mice rescues
the metabolic phenotype
Oh et al., 2015, Cell Reports 10, 1872–1886
March 24, 2015 ª2015 The Authors
http://dx./.
Cell Reports
Article
Deletion of Macrophage Vitamin D Receptor Promotes
Insulin Resistance and Monocyte Cholesterol
Transport to Accelerate Atherosclerosis in Mice
Jisu Oh,1,5 Amy E. Riek,1,5 Isra Darwech,1 Katsuhiko Funai,2 JianSu Shao,1 Kathleen Chin,1 Oscar L. Sierra,1
Geert Carmeliet,3 Richard E. Ostlund, Jr.,1 and Carlos Bernal-Mizrachi1,4,*
1Division of Endocrinology, Metabolism, and Lipid Research, Washington University School of Medicine, St. Louis, MO 63110, USA
2Department of Kinesiology and Physiology, East Carolina University, Greenville, NC 27858, USA
3Department of Clinical and Experimental Endocrinology, KU Leuven, 3000 Leuven, Belgium
4Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis,
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