scholarly journals A Role for PPARγin the Regulation of Cytokines in Immune Cells and Cancer

PPAR Research ◽  
2008 ◽  
Vol 2008 ◽  
pp. 1-12 ◽  
Author(s):  
Xiao Yi Yang ◽  
Li Hua Wang ◽  
William L. Farrar
Keyword(s):  
Immune Cells ◽  
Cellular Differentiation ◽  
Cytokine Production ◽  
Peroxisome Proliferator ◽  
Biological Functions ◽  
Inhibit Tumor Growth ◽  
Peroxisome Proliferator Activated Receptor ◽  
Nuclear Receptor Superfamily ◽  
Abundant Evidence ◽  
Important Regulator

Peroxisome proliferator-activated receptorγ(PPARγ) is a ligand-activated transcription factor and a member of the nuclear receptor superfamily. PPARγand its ligands appear to serve diverse biological functions. In addition to the well-studied effects of PPARγon metabolism and cellular differentiation, abundant evidence suggests that PPARγis an important regulator of the immune system and cancers. Since cytokines are not only key modulators of inflammation with pro- and anti-inflammatory functions but they also can either stimulate or inhibit tumor growth and progression, this review summarizes the role for PPARγin the regulation of cytokine production and cytokine-mediated signal transduction pathways in immune cells and cancer.

scholarly journals Role of Peroxisome Proliferator-Activated Receptor-γin Vascular Inflammation

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Kousei Ohshima ◽  
Masaki Mogi ◽  
Masatsugu Horiuchi
Keyword(s):  
Immune Cells ◽  
Adipocyte Differentiation ◽  
Therapeutic Potential ◽  
Vascular Inflammation ◽  
Experimental Studies ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Important Regulator ◽  
Artery Disease

Vascular inflammation plays a crucial role in atherosclerosis, and its regulation is important to prevent cerebrovascular and coronary artery disease. The inflammatory process in atherogenesis involves a variety of immune cells including monocytes/macrophages, lymphocytes, dendritic cells, and neutrophils, which all express peroxisome proliferator-activated receptor-γ(PPAR-γ). PPAR-γis a nuclear receptor and transcription factor in the steroid superfamily and is known to be a key regulator of adipocyte differentiation. Increasing evidence from mainly experimental studies has demonstrated that PPAR-γactivation by endogenous and synthetic ligands is involved in lipid metabolism and anti-inflammatory activity. In addition, recent clinical studies have shown a beneficial effect of thiazolidinediones, synthetic PPAR-γligands, on cardiovascular disease beyond glycemic control. These results suggest that PPAR-γactivation is an important regulator in vascular inflammation and is expected to be a therapeutic target in the treatment of atherosclerotic complications. This paper reviews the recent findings of PPAR-γinvolvement in vascular inflammation and the therapeutic potential of regulating the immune system in atherosclerosis.

scholarly journals Peroxisome Proliferator-Activated Receptor-γIs Critical to Cardiac Fibrosis

PPAR Research ◽  
2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Huang-Jun Liu ◽  
Hai-Han Liao ◽  
Zheng Yang ◽  
Qi-Zhu Tang
Keyword(s):  
Immune Cells ◽  
Molecular Mechanisms ◽  
Cardiac Fibrosis ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Nuclear Receptor Superfamily ◽  
Infarction Heart

Peroxisome proliferator-activated receptor-γ(PPARγ) is a ligand-activated transcription factor belonging to the nuclear receptor superfamily, which plays a central role in regulating lipid and glucose metabolism. However, accumulating evidence demonstrates that PPARγagonists have potential to reduce inflammation, influence the balance of immune cells, suppress oxidative stress, and improve endothelial function, which are all involved in the cellular and molecular mechanisms of cardiac fibrosis. Thus, in this review we discuss the role of PPARγin various cardiovascular conditions associated with cardiac fibrosis, including diabetes mellitus, hypertension, myocardial infarction, heart failure, ischemia/reperfusion injury, atrial fibrillation, and several other cardiovascular disease (CVD) conditions, and summarize the developmental status of PPARγagonists for the clinical management of CVD.

scholarly journals Flubendiamide Enhances Adipogenesis and Inhibits AMPKα in 3T3-L1 Adipocytes

Molecules ◽  
2018 ◽  
Vol 23 (11) ◽  
pp. 2950 ◽  
Author(s):  
Quancai Sun ◽  
Jie Lin ◽  
Yukui Peng ◽  
Ruichang Gao ◽  
Ye Peng
Keyword(s):  
Adipocyte Differentiation ◽  
Peroxisome Proliferator ◽  
Potential Influence ◽  
Peroxisome Proliferator Activated Receptor ◽  
Acetyl Coenzyme A ◽  
Enhancer Binding Protein ◽  
Triglyceride Content ◽  
Important Regulator ◽  
Amp Activated Protein Kinase ◽  
Acetyl Coenzyme A Carboxylase

Flubendiamide, a ryanoid class insecticide, is widely used in agriculture. Several insecticides have been reported to promote adipogenesis. However, the potential influence of flubendiamide on adipogenesis is largely unknown. The current study was therefore to determine the effects of flubendiamide on adipogenesis utilizing the 3T3-L1 adipocytes model. Flubendiamide treatment not only enhanced triglyceride content in 3T3-L1 adipocytes, but also increased the expression of cytosine-cytosine-adenosine-adenosine-thymidine (CCAAT)/enhancer-binding protein α and peroxisome proliferator-activated receptor gamma-γ, two important regulators of adipocyte differentiation. Moreover, the expression of the most important regulator of lipogenesis, acetyl coenzyme A carboxylase, was also increased after flubendiamide treatment. Further study revealed that 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) or A769662, two Adenosine 5′-monophosphate (AMP)-activated protein kinase α activators, subverted effects of flubendiamide on enhanced adipogenesis. Together, these results suggest that flubendiamide promotes adipogenesis via an AMPKα-mediated pathway.

scholarly journals Peroxisome Proliferator-Activated Receptor γ and PGC-1α in Cancer: Dual Actions as Tumor Promoter and Suppressor

PPAR Research ◽  
2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Seong-Hoon Yun ◽  
Sang-Heum Han ◽  
Joo-In Park
Keyword(s):  
Metabolic Pathways ◽  
Energy Homeostasis ◽  
Tumor Promoter ◽  
Clinical Implications ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Interacting Protein ◽  
Action Mechanisms ◽  
Important Regulator

Peroxisome proliferator-activated receptor γ (PPARγ) is part of a nuclear receptor superfamily that regulates gene expression involved in cell differentiation, proliferation, immune/inflammation response, and lipid metabolism. PPARγ coactivator-1α (PGC-1α), initially identified as a PPARγ-interacting protein, is an important regulator of diverse metabolic pathways, such as oxidative metabolism and energy homeostasis. The role of PGC-1α in diabetes, neurodegeneration, and cardiovascular disease is particularly well known. PGC-1α is also now known to play important roles in cancer, independent of the role of PPARγ in cancer. Though many researchers have studied the expression and clinical implications of PPARγ and PGC-1α in cancer, there are still many controversies about the role of PPARγ and PGC-1α in cancer. This review examines and summarizes some recent data on the role and action mechanisms of PPARγ and PGC-1α in cancer, respectively, particularly the recent progress in understanding the role of PPARγ in several cancers since our review was published in 2012.

scholarly journals A Role for PPARβ/δin Tumor Stroma and Tumorigenesis

PPAR Research ◽  
2008 ◽  
Vol 2008 ◽  
pp. 1-5 ◽  
Author(s):  
Rolf Müller ◽  
Martin Kömhoff ◽  
Jeffrey M. Peters ◽  
Sabine Müller-Brüsselbach
Keyword(s):  
Fatty Acid ◽  
Cellular Differentiation ◽  
Tumor Stroma ◽  
Endothelial Cell Proliferation ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Endogenous Fatty Acid ◽  
Blood Vessel Formation ◽  
Fatty Acid Catabolism

Peroxisome proliferator-activated receptor-β/δ(PPARβ/δ) is a transcription factor that is activated by endogenous fatty acid ligands and by synthetic agonists. Its role in the regulation of skeletal muscle fatty acid catabolism, glucose homeostasis, and cellular differentiation has been established in multiple studies. On the contrary, a role for PPARβ/δin tumorigenesis is less clear because there are contradictory reports in the literature. However, the majority of these studies have not examined the role of PPARβ/δin the tumor stroma. Recent evidence suggests that stromal PPARβ/δregulates tumor endothelial cell proliferation and promotes differentiation leading to the properly orchestrated events required for tumor blood vessel formation. This review briefly summarizes the significance of these studies that may provide clues to help explain the reported discrepancies in the literature regarding the role of PPARβ/δin tumorigenesis.

scholarly journals Critical role of peroxisome proliferator-activated receptor α in promoting platelet hyperreactivity and thrombosis under hyperlipidemia

Haematologica ◽  
2021 ◽  
Author(s):  
Li Li ◽  
Jiawei Zhou ◽  
Shuai Wang ◽  
Lei Jiang ◽  
Xiaoyan Chen ◽  
...  
Keyword(s):  
Platelet Activation ◽  
Thrombus Formation ◽  
Critical Role ◽  
Dense Granule ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Important Regulator ◽  
Dense Granule Secretion ◽  
Granule Secretion ◽  
Underlying Mechanisms

Platelet hyperreactivity and increased atherothrombotic risk are specifically associated with dyslipidemia. Peroxisome proliferator-activated receptor alpha (PPARα) is an important regulator of lipid metabolism. It was suggested to affect both thrombosis and hemostasis, yet the underlying mechanisms are not well understood. In this study, the role and mechanism of PPARα in platelet activation and thrombosis related to dyslipidemia were examined. Employing mice with deletion of PPARα (Pparα -/-), we demonstrated that PPARα is required for platelet activation and thrombus formation. The effect of PPARα is critically dependent on platelet dense granule secretion, and is contributed by p38MAPK/Akt, fatty acid β- oxidation, and NAD(P)H oxidase (NOX) pathways. Importantly, PPARα and the associated pathways mediated a prothrombotic state induced by high-fat diet (HFD) and platelet hyperactivity provoked by oxidized low density lipoproteins (oxLDL). Platelet reactivities were positively correlated with the expression levels of PPARα, as revealed by data from wild-type (WT), chimeric (Pparα +/-), and Pparα -/- mice. This positive correlation was recapitulated in platelets from hyperlipidemic patients. In a lipid-treated megakaryocytic cell line, lipid-induced reactive oxygen species (ROS)-NF-κB pathway was revealed to upregulate platelet PPARα in hyperlipidemia. These data suggested platelet PPARα critically mediates platelet activation and contributes to prothrombotic status under hyperlipidemia.

scholarly journals Propofol Suppresses Proinflammatory Cytokine Production by Increasing ABCA1 Expression via Mediation by the Long Noncoding RNA LOC286367

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Xin Ma ◽  
Teng Wang ◽  
Zhen-Long Zhao ◽  
Yu Jiang ◽  
Shu Ye
Keyword(s):  
Proinflammatory Cytokine ◽  
Noncoding Rna ◽  
Cytokine Production ◽  
Peroxisome Proliferator ◽  
Dependent Manner ◽  
Proinflammatory Cytokine Production ◽  
Peroxisome Proliferator Activated Receptor ◽  
Atp Binding Cassette Transporter ◽  
Abca1 Expression ◽  
Necrosis Factor

We previously reported that propofol upregulated the expression of ATP-binding cassette transporter subfamily A member 1 (ABCA1) via peroxisome proliferator-activated receptor gamma/liver X receptor in macrophage-derived foam cells. Here, we provide evidence that in addition to inducing ABCA1 expression, propofol represses proinflammatory cytokine production by increasing ABCA1 expression in a LOC286367-dependent manner. Western blot analysis showed that ABCA1 expression was elevated in macrophages by propofol treatment and this effect was markedly reduced by LOC286367 overexpression. Moreover, propofol treatment downregulated the production of the proinflammatory cytokines interleukin-6, tumor necrosis factor, and interferon gamma in lipopolysaccharide-stimulated macrophages by enhancing ABCA1 expression. Notably, propofol achieved this effect in a LOC286367-dependent manner. To the best of our knowledge, this is the first report of the mechanism in which propofol represses proinflammatory cytokine production mediated by ABCA1.

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