Unlike PPARγ, PPARα or PPARβ/δ activation does not promote human monocyte differentiation toward alternative macrophages

MA Bouhlel, J Brozek, B Derudas, C Zawadzki… - Biochemical and …, 2009 - Elsevier
MA Bouhlel, J Brozek, B Derudas, C Zawadzki, B Jude, B Staels, G Chinetti-Gbaguidi
Biochemical and biophysical research communications, 2009Elsevier
Macrophages adapt their response to micro-environmental signals. While Th1 cytokines
promote pro-inflammatory M1 macrophages, Th2 cytokines promote an “alternative” anti-
inflammatory M2 macrophage phenotype. Peroxisome proliferator-activated receptors
(PPARs) are ligand-activated transcription factors expressed in macrophages where they
control the inflammatory response. It has been shown that PPARγ promotes the
differentiation of monocytes into anti-inflammatory M2 macrophages in humans and mice …
Macrophages adapt their response to micro-environmental signals. While Th1 cytokines promote pro-inflammatory M1 macrophages, Th2 cytokines promote an “alternative” anti-inflammatory M2 macrophage phenotype. Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors expressed in macrophages where they control the inflammatory response. It has been shown that PPARγ promotes the differentiation of monocytes into anti-inflammatory M2 macrophages in humans and mice, while a role for PPARβ/δ in this process has been reported only in mice and no data are available for PPARα. Here, we show that in contrast to PPARγ, expression of PPARα and PPARβ/δ overall does not correlate with the expression of M2 markers in human atherosclerotic lesions, whereas a positive correlation with genes of lipid metabolism exists. Moreover, unlike PPARγ, PPARα or PPARβ/δ activation does not influence human monocyte differentiation into M2 macrophages in vitro. Thus, PPARα and PPARβ/δ do not appear to modulate the alternative differentiation of human macrophages.
Elsevier