PPARgamma activation primes human monocytes into alternative M2 macrophages with anti-inflammatory properties.

By Mohamed Amine Bouhlel, B. Derudas, E. Rigamonti, R. Dièvart, J. Brozek, S. Haulon, C. Zawadzki, B. Jude, G. Torpier, N. Marx and 2 more. Cell Metabolism, 2007

1,331 citations recorded by the source corpus.

Subfields: Epidemiology, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/853e5fd4575b1db72b01328fe3c1f7dde4fe0ee9

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. Peter Libby
2. P. Ridker
3. G. Hansson
4. A. Chawla
5. J. Odegaard
6. M. Jain
7. Alok Kumar
8. Qing-Wu Yang

In Immunology

1. Peter Libby
2. P. Ridker
3. G. Hansson
4. A. Chawla
5. J. Odegaard
6. L. Chávez-Galán
7. Xiangming Zou
8. M. O’Banion

In Molecular Biology

1. Peter Libby
2. P. Ridker
3. G. Hansson
4. S. Bensinger
5. L. Chávez-Galán
6. A. Chawla
7. Xiangming Zou
8. I. Garcia

Citations in the corpus

• Molecular Mechanisms That Influence the Macrophage M1–M2 Polarization Balance (2014, background): “Molecular determinants of M1–M2 polarization include members of the PPAR, KLF, IRF, STAT, NF-κB, and HIF families, and miRNAs.”
• Alternative M2 activation of Kupffer cells by PPARdelta ameliorates obesity-induced insulin resistance. (2008, background): “On the one hand, attenuation of tissue inflammation by paracrine actions of these cells might lead to improvement in insulin signaling (Bouhlel et al., 2007).”
• Macrophage activation and its role in repair and pathology after spinal cord injury. (2015, background): “PPARγ transactivates M2 genes (e.g. CD206) by binding to the PPAR-responsive element (PPRE) sequence motif (Nicholson, 2004; Bouhlel et al., 2007).”
• Much More than M1 and M2 Macrophages, There are also CD169+ and TCR+ Macrophages (2015, methodology): “Peroxisome proliferator-activated receptor γ (PPARγ), a nuclear receptor with anti-inflammatory properties, has been proposed to enhance the M2 phenotype; however, only native monocytes can be primed by PPARγ, but not M2 resting or M1 macrophages (103).”
• Integration of metabolism and inflammation by lipid-activated nuclear receptors (2008, methodology): “The importance of PPAR-γ in regulating the M1/M2 macrophage switch was reconfirmed by recent work by Amine Bouhlel et al”
• Phenotypic Switching of Adipose Tissue Macrophages With Obesity Is Generated by Spatiotemporal Differences in Macrophage Subtypes (2008, neutral): “This is similar to what has been proposed to mediate monocyte/macrophage recruitment to atherosclerotic plaques (24,25).”
• Neuroinflammation and M2 microglia: the good, the bad, and the inflamed (2014, background): “Interestingly, PPARγ treatment has been demonstrated to polarize human monocytes to an M2 state [138], which further supports the idea that manipulating proinflammatory M1 microglia to an M2 phenotype is a potentially viable therapeutic option.”
• Transcriptional regulation of macrophage polarization: enabling diversity with identity (2011, background): “More recent studies have shown that PPARγ-deficient macrophages are resistant to M2 polarization and promote insulin resistanc”
• Krüppel-like factor 4 regulates macrophage polarization. (2011, background): “In addition, PPARγ has been shown to be induced by M2 stimuli in macrophages and thereby promote the M2 phenotype (4, 17, 30).”
• A CREB-C/EBPβ cascade induces M2 macrophage-specific gene expression and promotes muscle injury repair (2009, background): “However, the role of PPAR remains controversial, as PPAR activation has been observed to promote M2 polarization in adipose tissue (8).”
• PPARs are a unique set of fatty acid regulated transcription factors controlling both lipid metabolism and inflammation (2011, background): “who demonstrated that the level of M2 macrophages in atherosclerotic lesions correlated with the expression level of PPARγ [81].”
• Macrophage Polarization in Inflammatory Diseases (2014, background): “Many key transcription factors are involved in macrophage polarization[12], like signal transducer and activator of transcription (STATs)[13], interferon-regulatory factor (IRFs)[14, 15], nuclear factor (NF)-κB [16], activator protein (AP) 1 [17], peroxisome proliferator-activated receptor (PPAR)-γ ”