PPARα blocks glucocorticoid receptor α-mediated transactivation but cooperates with the activated glucocorticoid receptor α for transrepression on NF-κB

Proceedings of the National Academy of Sciences of the United States of America

Volumn 106, Issue 18, 2009, Pages 7397-7402

  Bougarne, Nadia ^a   Paumelle, Réjane ^b   Caron, Sandrine ^b   Hennuyer, Nathalie ^b   Mansouri, Roxane ^b   Gervois, Philippe ^b   Staels, Bart ^b   Haegeman, Guy ^a   De Bosscher, Karolien ^a  

^a GHENT UNIVERSITY   (Belgium)

^b UNIV LILLE   (France)

Author keywords

Cross talk; Gluconeogenesis; Hyperinsulinema side effects; Inflammation

Indexed keywords

2 [4 [2 [3 (2,4 DIFLUOROPHENYL) 1 HEPTYLUREIDO]ETHYL]PHENYLTHIO] 2 METHYLPROPIONIC ACID; DEXAMETHASONE; FENOFIBRATE; GLUCOCORTICOID; GLUCOCORTICOID RECEPTOR ALPHA; GW 647; IMMUNOGLOBULIN ENHANCER BINDING PROTEIN; INTERLEUKIN 6; PEROXISOME PROLIFERATOR ACTIVATED RECEPTOR AGONIST; PEROXISOME PROLIFERATOR ACTIVATED RECEPTOR ALPHA; PIRINIXIC ACID; RNA POLYMERASE II; TUMOR NECROSIS FACTOR ALPHA; UNCLASSIFIED DRUG; GLUCOCORTICOID RECEPTOR;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANTIINFLAMMATORY ACTIVITY; ARTICLE; CONTROLLED STUDY; CYTOKINE PRODUCTION; DOSE RESPONSE; DOWN REGULATION; DRUG INHIBITION; EMBRYO; FEMALE; GENE EXPRESSION; GENE REPRESSION; HUMAN; HUMAN CELL; HYPERINSULINEMIA; IMMUNOMODULATION; KNOCKOUT MOUSE; LIPID DIET; MALE; MOLECULAR INTERACTION; MOUSE; NONHUMAN; PHARMACOLOGICAL BLOCKING; PRIORITY JOURNAL; PROMOTER REGION; TRANSACTIVATION; TRANSCRIPTION REGULATION; WILD TYPE; ANIMAL; CHEMICALLY INDUCED DISORDER; DRUG ANTAGONISM; DRUG EFFECT; DRUG POTENTIATION; FAT INTAKE; GENETICS; HYPERINSULINISM; LIVER CELL; METABOLISM; MOUSE MUTANT; TRANSCRIPTION INITIATION; TUMOR CELL LINE;

MUS;

ANIMALS; CELL LINE, TUMOR; DIETARY FATS; GENE EXPRESSION; GLUCOCORTICOIDS; HEPATOCYTES; HUMANS; HYPERINSULINISM; MICE; MICE, KNOCKOUT; NF-KAPPA B; PPAR ALPHA; PROCETOFEN; PROMOTER REGIONS, GENETIC; RECEPTORS, GLUCOCORTICOID; TRANSCRIPTIONAL ACTIVATION;

EID: 66149149061     PISSN: 00278424     EISSN: 10916490     Source Type: Journal    
DOI: 10.1073/pnas.0806742106     Document Type: Article

References (21)

1. De Bosscher K, Vanden Berghe W, Haegeman G (2003) The interplay between the GR and NF-κB or AP-1: Molecular mechanisms for gene repression. EndocrRev 24:488-522.
2. Shiri-Sverdlov R, etal. (2006) Early diet-induced non-alcoholic steatohepatitis in APOE2 knockin mice and its prevention by fibrates. J Hepatol 44:732-741.
3. Desvergne B, Wahli W (1999) PPARs: Nuclear control of metabolism. Endocr Rev 20:649-688.
4. Delerive P, et al. (1999) PPARα negatively regulates the vascular inflammatory gene response by negative cross-talk with transcription factors NF-κB and AP-1. J Biol Chem 274:32048-32054.
5. Staels B, et al. (1998) Activation of human aortic smooth-muscle cells is inhibited by PPARα but not by PPARγ activators. Nature 393:790-793.
6. Guerre-Millo M, et al. (2000) PPARα activators improve insulin sensitivity and reduce adiposity. J Biol Chem 275:16638-16642.
7. Barthel A, Schmoll D (2003) Novel concepts in insulin regulation of hepatic gluconeogenesis. Am J Physiol 285:E685-E692.
8. Kajimura S, et al. (2008) Regulation of the brown and white fat programs through a PRDM16/CtBP transcriptional complex. Genes Dev 22:1397-1409.
9. De Bosscher K, et al. (2005) A fully dissociated compound of plant origin for inflammatorygene repression. ProcNatl Acad Sci USA102:15827-15832.
10. Newton R, Holden NS (2007) Separating transrepression and transactivation: A distressing divorce for the GR? Mol Pharmacol 72:799-809.
11. Cuzzocrea S, et al. (2008) PPARα contributes to the anti-inflammatory activity of glucocorticoids. Mol Pharmacol 73:323-337.
12. Sutherland C, O'Brien RM, Granner DK (1996) New connections in the regulation of PEPCK gene expression byinsulin. Philos TransR SocLondon SerB 351:191-199.
13. Pierreux CE, et al. (1998) inhibition by insulin of GC-induced gene transcription: involvement of the ligand-binding domain of the GR and independence from the PI3-kinase and MAPK pathways. Mol Endocrinol 12:1343-1354.
14. Bernal-Mizrachi C, etal. (2003)Dexamethasone induction ofhypertension and diabetes is PPARa dependent in LDL receptor-null mice. Nat Med 9:1069-1075.
15. Subramanian S, et al. (2006) PPARa activation elevates blood pressure and does not correctGC-induced insulin resistance in humans. Am JPhysiol291:E1365-E1371.
16. OgawaS,etal. (2005)Moleculardeterminantsofcross-talkbetween nuclearreceptors and toll-like receptors. Cell122:707-721.
17. Chinetti G, Fruchart JC, Staels B (2003) PPAR-activated receptors: New targets for the pharmacological modulation ofmacrophagegeneexpression andfunction. CurrOpin Lipidol 14:459-468.
18. Berry MN, Friend DS (1969) High-yield preparation of isolated rat liver parenchymal cells: A biochemical and fine structural study. J Cell Biol 43:506-520.
19. Wong C, et al. (1999) Smad3-Smad4 and AP-1 complexes synergize in transcriptional activation of the c-Jun promoter by TGFβ. Mol Cell Biol 19:1821-1830.
20. Adcock IM, Nasuhara Y, Stevens DA, Barnes PJ (1999) Ligand-induced differentiation of GRtransrepression and transactivation: Preferential targetting of NF-κB and lack of I-κB involvement. Br J Pharmacol 127:1003-1011.
21. Wang JC, et al. (2004) Chromatin immunoprecipitation (ChIP) scanning identifies primaryGR targetgenes. ProcNatlAcad SciUSA101:15603-15608.