High impact information on PPARG

• We previously reported that laminar flow activates peroxisome proliferator-activated receptor gamma (PPARgamma) in vascular endothelial cells in a ligand-dependent manner that involves phospholipase A2 and cytochrome P450 epoxygenases [1].
• This phenotype appears to be related to the induction of the transcription factor peroxisome proliferator-activated receptor gamma (PPARgamma), since DEF-1 NIH 3T3 cells demonstrated augmented levels of PPARgamma mRNA and, when treated with activating PPARgamma ligands, efficient induction of differentiation [2].
• Reduction in the evolution of murine type II collagen-induced arthritis by treatment with rosiglitazone, a ligand of the peroxisome proliferator-activated receptor gamma [3].
• OBJECTIVE: The peroxisome proliferator-activated receptor gamma (PPARgamma) is a member of the nuclear receptor superfamily of ligand-dependent transcription factors related to retinoid, steroid, and thyroid hormone receptors [3].
• Cotyledonary and caruncular tissues were obtained for quantification of vascular endothelial growth factor (VEGF) and peroxisome proliferator-activated receptor-gamma (PPARgamma) mRNA and protein [4].

Biological context of PPARG

• Using genetic linkage analysis we have also assigned the PPAR gamma gene to bovine chromosome 22 [5].
• The cell cycle (S phase portion in cells on days 5, 12 and 20: 16 +/- 4%, 6 +/- 4% and 4 +/- 3%, respectively) and the portion of cells with PCNA correlated with the amount of PPAR-gamma in non-pregnant heifers [6].
• ATA promoted the S phase in cells of non-pregnant heifers (day 12) and the endogenous agonist of PPAR-gamma, 15dPGJ2, inhibited the response to ATA in a dose-dependent manner, indicating that PPAR-gamma plays a role in the arrest of the cell cycle in lutein cells to maintain their differentiated state [6].
• The adipocyte differentiation process involves a cascade of transcriptional events that culminates in the expression of peroxisome proliferator-activated receptor-gamma (PPARgamma) and CCAAT/enhancer binding protein-alpha (C/EBPalpha) [7].

Anatomical context of PPARG

• PPAR gamma 1 was expressed at relatively high levels in bovine spleen and lung and to a lower extent in ovary, mammary gland, and small intestine [5].
• In this study, we investigated the role of troglitazone, a potent agonist of peroxisome proliferator activated receptor-gamma (PPARgamma) used for the treatment of diabetes, on the NO release and the effect of exposure to high glucose on the production of NO in cultured bovine retinal pericytes [8].
• Dexamethasone, a lipid supplement (Excyte) and the thiazolidinedione, rosiglitazone (BRL 49653) (a peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonist) all enhanced preadipocyte differentiation, whereas fibroblast growth factor and GH were inhibitory [9].
• Oxidized LDL binding to LOX-1 upregulates VEGF expression in cultured bovine chondrocytes through activation of PPAR-gamma [10].
• Peroxisome proliferator-activated receptor gamma may play an important role in adipocyte differentiation, and retinoids may interfere with the action of PPARgamma in cattle [11].

Associations of PPARG with chemical compounds

• OBJECTIVE: This study compares the effects of the thiazolidinedione, troglitazone (TGZ), dexamethasone (DEX), and DEX plus TGZ on preadipocyte differentiation and the expression of CCAAT/enhancer-binding protein-alpha (C/ EBPalpha) and peroxisome proliferator-activated receptor-gamma (PPARgamma) [12].
• The compounds are thought to function as direct activators of the nuclear receptor PPARgamma (peroxisome proliferator-activated receptor-gamma), although pioglitazone, the weaker agonist of the two thiazolidinediones now in clinical use, seems to have more useful effects on circulating lipids [13].
• Detection and functional characterisation of the transcription factor peroxisome proliferator-activated receptor gamma in lutein cells [14].
• The specific PPAR-gamma inhibitor GW9662 suppressed ox-LDL-induced VEGF expression [10].
• The response of the cells to PPAR-gamma agonist 15-deoxy-delta 12,14 prostaglandin J2 (15dPGJ2, 200 and 490 nmol l-1) with and without changing the cell cycle by the anti-apoptogenic drug aurintricarboxylic acid (ATA, 10 mumol l-1) was used as an in vitro model to study the relationship between the cell cycle and PPAR-gamma [6].

Enzymatic interactions of PPARG

• This study shows that both PPAR-alpha (Wy 14643) and PPAR-gamma activation (rosiglitazone) partially inhibit oxidized LDL-induced protein kinase C activity and endothelin-1 secretion in endothelial cells at the transcriptional levels and suggests that synthetic PPAR activators are stronger PPAR activators than oxidized LDL [15].

Regulatory relationships of PPARG

• Oxidized low-density lipoproteins (LDLs) induce atherosclerosis in the vascular wall, as well as endothelin-1 secretion in endothelial cells and are activators of both peroxisome proliferator-activated receptor-alpha (PPAR-alpha) and PPAR-gamma [15].

Other interactions of PPARG

• Physical and genetic mapping of bovine CEBPA and PPARG genes [16].
• Relationship between different stages of the corpus luteum and the expression of the peroxisome proliferator-activated receptor gamma protein in bovine large lutein cells [6].

Analytical, diagnostic and therapeutic context of PPARG

• The distribution of PPAR gamma mRNAs in various bovine tissues was investigated using Northern blot analysis [5].
• PPAR-gamma in single cells was analysed by flow cytometry [6].
• PPAR-gamma 1 and PPAR-gamma 2 isoforms were distinguished by immunoblotting [6].

References