Abstract
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 PPAR{gamma} promotes the differentiation of monocytes into anti-inflammatory M2 macrophages in humans and mice, while a role for PPAR{beta}/{delta} in this process has been reported only in mice and no data are available for PPAR{alpha}. Here, we show that in contrast to PPAR{gamma}, expression of PPAR{alpha} and PPAR{beta}/{delta} 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 PPAR{gamma}, PPAR{alpha} or PPAR{beta}/{delta} activation does not influence human monocyte differentiation into M2 macrophages in vitro. Thus, PPAR{alpha} and PPAR{beta}/{delta} do not appear to modulate the alternative differentiation of human macrophages.
Bouhlel, Mohamed Amine;
[1]
Inserm U545, F-59000 Lille;
[2]
UDSL, F-59000 Lille;
[2]
Institut Pasteur de Lille, F-59019 Lille (France)];
Brozek, John;
[3]
Derudas, Bruno;
[1]
Inserm U545, F-59000 Lille;
[2]
UDSL, F-59000 Lille;
[2]
Institut Pasteur de Lille, F-59019 Lille (France)];
Zawadzki, Christophe;
Jude, Brigitte;
[4]
Staels, Bart;
[1]
Inserm U545, F-59000 Lille;
[2]
UDSL, F-59000 Lille;
[2]
Institut Pasteur de Lille, F-59019 Lille (France)];
Chinetti-Gbaguidi, Giulia;
[1]
Inserm U545, F-59000 Lille;
[2]
UDSL, F-59000 Lille;
[2]
Institut Pasteur de Lille, F-59019 Lille (France)]
- Univ Lille Nord de France, F-59000 Lille (France)
- France
- Genfit, Loos (France)
- Inserm ERI-9 and Equipe d'Accueil 2693, IFR114, Universite de Lille, Lille (France)
Citation Formats
Bouhlel, Mohamed Amine, Inserm U545, F-59000 Lille, UDSL, F-59000 Lille, Institut Pasteur de Lille, F-59019 Lille (France)], Brozek, John, Derudas, Bruno, Inserm U545, F-59000 Lille, UDSL, F-59000 Lille, Institut Pasteur de Lille, F-59019 Lille (France)], Zawadzki, Christophe, Jude, Brigitte, Staels, Bart, Inserm U545, F-59000 Lille, UDSL, F-59000 Lille, Institut Pasteur de Lille, F-59019 Lille (France)], Chinetti-Gbaguidi, Giulia, Inserm U545, F-59000 Lille, UDSL, F-59000 Lille, and Institut Pasteur de Lille, F-59019 Lille (France)].
Unlike PPAR{gamma}, PPAR{alpha} or PPAR{beta}/{delta} activation does not promote human monocyte differentiation toward alternative macrophages.
United States: N. p.,
2009.
Web.
doi:10.1016/J.BBRC.2009.06.047.
Bouhlel, Mohamed Amine, Inserm U545, F-59000 Lille, UDSL, F-59000 Lille, Institut Pasteur de Lille, F-59019 Lille (France)], Brozek, John, Derudas, Bruno, Inserm U545, F-59000 Lille, UDSL, F-59000 Lille, Institut Pasteur de Lille, F-59019 Lille (France)], Zawadzki, Christophe, Jude, Brigitte, Staels, Bart, Inserm U545, F-59000 Lille, UDSL, F-59000 Lille, Institut Pasteur de Lille, F-59019 Lille (France)], Chinetti-Gbaguidi, Giulia, Inserm U545, F-59000 Lille, UDSL, F-59000 Lille, & Institut Pasteur de Lille, F-59019 Lille (France)].
Unlike PPAR{gamma}, PPAR{alpha} or PPAR{beta}/{delta} activation does not promote human monocyte differentiation toward alternative macrophages.
United States.
https://doi.org/10.1016/J.BBRC.2009.06.047
Bouhlel, Mohamed Amine, Inserm U545, F-59000 Lille, UDSL, F-59000 Lille, Institut Pasteur de Lille, F-59019 Lille (France)], Brozek, John, Derudas, Bruno, Inserm U545, F-59000 Lille, UDSL, F-59000 Lille, Institut Pasteur de Lille, F-59019 Lille (France)], Zawadzki, Christophe, Jude, Brigitte, Staels, Bart, Inserm U545, F-59000 Lille, UDSL, F-59000 Lille, Institut Pasteur de Lille, F-59019 Lille (France)], Chinetti-Gbaguidi, Giulia, Inserm U545, F-59000 Lille, UDSL, F-59000 Lille, and Institut Pasteur de Lille, F-59019 Lille (France)].
2009.
"Unlike PPAR{gamma}, PPAR{alpha} or PPAR{beta}/{delta} activation does not promote human monocyte differentiation toward alternative macrophages."
United States.
https://doi.org/10.1016/J.BBRC.2009.06.047.
@misc{etde_22199774,
title = {Unlike PPAR{gamma}, PPAR{alpha} or PPAR{beta}/{delta} activation does not promote human monocyte differentiation toward alternative macrophages}
author = {Bouhlel, Mohamed Amine, Inserm U545, F-59000 Lille, UDSL, F-59000 Lille, Institut Pasteur de Lille, F-59019 Lille (France)], Brozek, John, Derudas, Bruno, Inserm U545, F-59000 Lille, UDSL, F-59000 Lille, Institut Pasteur de Lille, F-59019 Lille (France)], Zawadzki, Christophe, Jude, Brigitte, Staels, Bart, Inserm U545, F-59000 Lille, UDSL, F-59000 Lille, Institut Pasteur de Lille, F-59019 Lille (France)], Chinetti-Gbaguidi, Giulia, Inserm U545, F-59000 Lille, UDSL, F-59000 Lille, and Institut Pasteur de Lille, F-59019 Lille (France)]}
abstractNote = {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 PPAR{gamma} promotes the differentiation of monocytes into anti-inflammatory M2 macrophages in humans and mice, while a role for PPAR{beta}/{delta} in this process has been reported only in mice and no data are available for PPAR{alpha}. Here, we show that in contrast to PPAR{gamma}, expression of PPAR{alpha} and PPAR{beta}/{delta} 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 PPAR{gamma}, PPAR{alpha} or PPAR{beta}/{delta} activation does not influence human monocyte differentiation into M2 macrophages in vitro. Thus, PPAR{alpha} and PPAR{beta}/{delta} do not appear to modulate the alternative differentiation of human macrophages.}
doi = {10.1016/J.BBRC.2009.06.047}
journal = []
issue = {3}
volume = {386}
journal type = {AC}
place = {United States}
year = {2009}
month = {Aug}
}
title = {Unlike PPAR{gamma}, PPAR{alpha} or PPAR{beta}/{delta} activation does not promote human monocyte differentiation toward alternative macrophages}
author = {Bouhlel, Mohamed Amine, Inserm U545, F-59000 Lille, UDSL, F-59000 Lille, Institut Pasteur de Lille, F-59019 Lille (France)], Brozek, John, Derudas, Bruno, Inserm U545, F-59000 Lille, UDSL, F-59000 Lille, Institut Pasteur de Lille, F-59019 Lille (France)], Zawadzki, Christophe, Jude, Brigitte, Staels, Bart, Inserm U545, F-59000 Lille, UDSL, F-59000 Lille, Institut Pasteur de Lille, F-59019 Lille (France)], Chinetti-Gbaguidi, Giulia, Inserm U545, F-59000 Lille, UDSL, F-59000 Lille, and Institut Pasteur de Lille, F-59019 Lille (France)]}
abstractNote = {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 PPAR{gamma} promotes the differentiation of monocytes into anti-inflammatory M2 macrophages in humans and mice, while a role for PPAR{beta}/{delta} in this process has been reported only in mice and no data are available for PPAR{alpha}. Here, we show that in contrast to PPAR{gamma}, expression of PPAR{alpha} and PPAR{beta}/{delta} 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 PPAR{gamma}, PPAR{alpha} or PPAR{beta}/{delta} activation does not influence human monocyte differentiation into M2 macrophages in vitro. Thus, PPAR{alpha} and PPAR{beta}/{delta} do not appear to modulate the alternative differentiation of human macrophages.}
doi = {10.1016/J.BBRC.2009.06.047}
journal = []
issue = {3}
volume = {386}
journal type = {AC}
place = {United States}
year = {2009}
month = {Aug}
}