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"In primary cultured rat hippocampal neurons Abeta 1-42 treatment significantly enhanced PPARgamma phosphorylation at Ser273, increased the p-PPARgamma and PPARgamma ratio and decreased PPARgamma protein and mRNA expression levels compared with those in the control group (P < 0.05; XREF_FIG)."
| PMC
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"Furthermore, curcumin increases the expression of PPARgamma and promotes nuclear translocation of PPARgamma in IEC-6 cells (XREF_FIG) and these results confirmed the previous reports that curcumin activated PPARgamma which was regarded as PPARgamma agonist [XREF_BIBR, XREF_BIBR, XREF_BIBR]."
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"Although this study did not demonstrate that p38 directly regulates the phosphorylation levels of PPAR-γ and blocks proteasomal degradation, numerous studies have reported that the activation of p38 can increase the phosphorylation levels of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), thereby enhancing the stability of PPAR-γ (Fei et al., 2012; Wang et al., 2016)."
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"Overexpression of visfatin/PBEF/Nampt also results in the upregulation of PPARg and SREBP2 mRNA levels.Visfatin upregulates PPARg and SREBP-2 317Visfatin/PBEF/Nampt overexpressing rats were generated by intramuscular injection of a plasmid vector (pcDNA3.1-visfatin) containing a mouse visfatin/PBEF/Nampt cDNA."
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"Peroxisome-proliferator activated receptor gamma (PPARgamma), a transcription factor (TF) controlling adipocyte differentiation, was demonstrated to function as a crucial TF in inhibiting HSC activation 11, 12 and ectopic expression of PPARgamma can cause the morphological and biochemical reversal of activated HSCs to quiescent cells 13."
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"Inhibition of PPAR-γ expression reversed these trends, underscoring the regulatory role of PPAR-γ in neutrophil polarization and the anti-inflammatory effects mediated by hMSCs.Subsequently, we evaluated the effects of secreted factors from hMSCs on the PPAR-γ/STAT6/SOCS1 signaling pathways through both in vitro and in vivo experiments."
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"Indeed, certain growth factors, cytokines and stress conditions repress PPARg 's transcriptional activity and impair adipogenesis by inducing the phosphorylation of PPARg on Ser112 via mitogen activated protein kinases (MAPK) / extracellular-signal regulated kinases 1 and 2 (ERK1/2),15 or the stress activated MAPKs JNK and p38.16,17 In contrast, PPARg phosphorylation on the same site by the cyclin dependent kinases Cdk7 and Cdk9 promotes PPARg activity, further illustrating the complexity of the regulation of PPARg by phosphorylation."
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"If this is the case, it will be important to determine from a nutritional point of view whether such natural molecules could selectively trigger different PPARgamma signaling, including the regulation of FGFs, the activation of PPARgamma in the brain or the phosphorylation of PPARgamma by Cdk5."
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"By tracking cells and monitoring expression of PPARG in individual cells over the time course of DMI-induced adipogenesis, we showed that PPARG expression during adipogenesis can be divided into 3 sequential phases with DMI mediating a linear increase in PPARG in Phase 1, positive feedback starting to engage in Phase 2 and ending with PPARG levels reaching a critical threshold where self-amplification takes over and the external input stimulus is not needed any more."
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"Simultaneously, chrysin significantly increased the mRNA levels of PPARgamma, liver X receptor alpha (LXRalpha), ATP binding cassette, sub-family A1 (ABCA1), and sub-family G1 (ABCG1), decreased scavenger receptor A1 (SR-A1) and SR-A2, and increased the transcriptional activity of PPARgamma."
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"6 C The Authors Journal compilation C 2010 Portland Press Ltd
Regulation of adipogenesis by STAT3 via PPARγ
Research article
Figure 5 STAT3 mediates adipocyte differentiation via PPARγ activation Activation of PPARγ by TAZ abolished stattic-mediated suppression of adipocyte differentiation (A and B)."
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"Likewise, Li et al. [55] demonstrated the prevention of lipid droplet accumulation in mouse 3T3-L1 preadipocytes following VD3 treatment (1 µM, 60 h), attributing the anti-adipogenic effect to the capacity to decrease the expression of PPAR-γ1.An overexpression of PPAR-γ1 leads to an upregulation of CD-36, a protein transporter recognized to promote the cellular uptake of ox-LDL and FFA."
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"While we showed that the increased adiponectin mRNA and serum concentrations were not a result of increased PPARgamma gene expression, others have shown that in vitro, niacin increases PPARgamma mRNA expression XREF_BIBR, XREF_BIBR, induces nuclear expression of PPARgamma protein and enhances PPARgamma transcriptional activity XREF_BIBR."
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"It is clear that there is crosstalk during heterotypic differentiation, such as the reciprocal relationship between adipogenic and endotheliogenic fates mediated by VEGF [35, 36] or adipogenic and osteogenic fate mediated by peroxisome proliferator-activated receptor gamma (PPAR-γ) [37]."
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"Ligand dependent SUMOylation of PPARgamma at K395 promotes the interaction of PPARgamma with NCoR and histone deacetylase-3 (HDAC3) complexes on NF-kappaB inflammatory gene promoters, and it prevents ubiquitination and proteosomal degradation of the repressor complex, and sustains repression XREF_BIBR."
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"Previous study reported that PPAR-gamma expression could be decreased by TGF-beta1 via smad binding with the PPAR-gamma gene promoter to reduce the promoter activity of PPAR-gamma gene or through increasing the binding of histone deacetylase 1 (HDAC1) and decreasing the levels of acetylated histone3 (AcH3) at the PPAR-gamma promoter."
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"Our results in Figure 4 supported that activation of Ffar2 by butyric acid produced by L. mesenteroides EH-1 was a key event that suppressed the HFD-induced PPAR-γ expression and abdominal fats.The expression of PPAR-γ prior to other transcription factors in adipocytes modulates the adipogenesis in exponentially growing fibroblast cell lines, demonstrating the significance of PPAR-γ in the regulation of adipocyte differentiation [35]."
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"In agreement with the Oil Red O staining experiments in XREF_FIG, we found that treatment of cells with either metformin or A769662 effectively suppressed IID- and PIO stimulated increases in PPARgamma protein levels (XREF_FIG A and B), as well as IID- and PIO stimulated PPARgamma activity (XREF_FIG C), as determined by gene reporter assays."
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"In this regard, clinical and animal studies indicate that DM is a protective factor against the development of acute respiratory distress syndrome (ARDS); this phenomenon is mediated by, among other factors, an increase in the expression of peroxisome proliferator activated receptor gamma (PPAR-gamma), which may be overexpressed in patients with DM."
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"Moreover, this hypothesis is supported by work demonstrating that STAT5 induces PPARgamma expression in coordination with C/EBPbeta/delta and also directly stimulates PPARgamma transcriptional activity [XREF_BIBR], thus suggesting that STAT5 activation drives adipogenesis by inducing PPARgamma expression and activity."
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"Following inflammatory insult, endogenous IL-4 interacts with microglial IL-4 receptors, thereby increasing the production of Gal-3 and subsequently inducing the canonical transcriptional factor PPAR-γ leading to anti-inflammatory signaling (Figure 2), as described in Section “Peroxisome Proliferator-Activated Receptor Gamma Mediated Pathway” (15, 201)."
eidos
"PPARgamma is abundant in immune-related cell types , particularly in adipocytes , macrophages , dendritic cells , and microglia ( Yuan et al ., 2015 ; Villapol , 2018 ) , and is indicated as a key regulator of anti-inflammatory functions of microglia , because PPARgamma activation increases anti-inflammatory-related gene expression and down-regulates pro-inflammatory mediators in activated microglia / macrophages and promotes phagocytosis of apoptotic cells , contributing to the resolution of inflammation ( Flores et al ., 2016 ; Savage et al ., 2015 ; Villapol , 2018 ; Yamanaka et al ., 2012 ; Zhao et al ., 2015b ) , although there is a report showing that an antagonist of PPARgamma promotes the pro-inflammatory to anti-inflammatory phenotypic shift in LPS-treated microglia ( Ji et al ., 2018 ) ."