The role of PPAR-γ in macrophage differentiation and cholesterol uptake
Author: ["Kathryn J. Moore","Evan D. Rosen","Michael L. Fitzgerald","Felix Randow","Lorna P. Andersson","David Altshuler","David S. Milstone","Richard M. Mortensen","Bruce M. Spiegelman","Mason W. Freeman"]
Publication: Nature Medicine
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Abstract
Peroxisome proliferator-activated receptor-γ (PPAR-γ), the transcription factor target of the anti-diabetic thiazolidinedione (TZD) drugs, is reported to mediate macrophage differentiation and inflammatory responses. Using PPAR-γ–deficient stem cells, we demonstrate that PPAR-γ is neither essential for myeloid development, nor for such mature macrophage functions as phagocytosis and inflammatory cytokine production. PPAR-γ is required for basal expression of CD36, but not for expression of the other major scavenger receptor responsible for uptake of modified lipoproteins, SR-A. In wild-type macrophages, TZD treatment divergently regulated CD36 and class A macrophage-scavenger receptor expression and failed to induce significant cellular cholesterol accumulation, indicating that TZDs may not exacerbate macrophage foam-cell formation.
Cite this article
Moore, K., Rosen, E., Fitzgerald, M. et al. The role of PPAR-γ in macrophage differentiation and cholesterol uptake. Nat Med 7, 41–47 (2001). https://doi.org/10.1038/83328
