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Titolo:
RETINOIDS INCREASE HUMAN APO C-III EXPRESSION AT THE TRANSCRIPTIONAL LEVEL VIA THE RETINOID-X-RECEPTOR - CONTRIBUTION TO THE HYPERTRIGLYCERIDEMIC ACTION OF RETINOIDS
Autore:
VUDAC N; GERVOIS P; TORRA IP; FRUCHART JC; KOSYKH V; KOOISTRA T; PRINCEN HMG; DALLONGEVILLE J; STAELS B;
Indirizzi:
INST PASTEUR,DEPT ATHEROSCLEROSE,INSERM,U325,1 RUE CALMETTE F-59019 LILLE FRANCE INST PASTEUR,DEPT ATHEROSCLEROSE,INSERM,U325 F-59019 LILLE FRANCE UNIV LILLE 2,FAC PHARM F-59006 LILLE FRANCE CARDIOL RES COMPLEX MOSCOW 121552 RUSSIA TNO PG,GAUBIUS LAB NL-2301 CE LEIDEN NETHERLANDS
Titolo Testata:
The Journal of clinical investigation
fascicolo: 3, volume: 102, anno: 1998,
pagine: 625 - 632
SICI:
0021-9738(1998)102:3<625:RIHACE>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
APOLIPOPROTEIN-A-I; TRIGLYCERIDE-RICH LIPOPROTEINS; CIII GENE-EXPRESSION; TRANSGENIC MICE; LOW-DENSITY; SELECTIVE RETINOIDS; SERUM-LIPOPROTEINS; ACID RECEPTOR; ISOTRETINOIN; METABOLISM;
Keywords:
GENE REGULATION; TRIGLYCERIDES; HYPERLIPIDEMIA; RETINOIDS; NUCLEAR RECEPTORS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
62
Recensione:
Indirizzi per estratti:
Citazione:
N. Vudac et al., "RETINOIDS INCREASE HUMAN APO C-III EXPRESSION AT THE TRANSCRIPTIONAL LEVEL VIA THE RETINOID-X-RECEPTOR - CONTRIBUTION TO THE HYPERTRIGLYCERIDEMIC ACTION OF RETINOIDS", The Journal of clinical investigation, 102(3), 1998, pp. 625-632

Abstract

Hypertriglyceridemia is a metabolic complication of retinoid therapy. In this study, we analyzed whether retinoids increase the expression of apo C-III, an antagonist of plasma triglyceride catabolism. In men,isotretinoin treatment (80 mg/d; 5 d) resulted in elevated plasma apoC-III, but not apo E concentrations. In human hepatoma HepG2 cells, retinoids increased apo C-III mRNA and protein production. Transient transfection experiments indicated that retinoids increase apo C-III expression at the transcriptional level. This increased apo C-III transcription is mediated by the retinoid X receptor (RXR), since LG1069 hydro-3,5,5,8,8-pentamethyl-2-naphtalenyl)ethenyl] benzoic acid), a RXR-specific agonist, but not TTNPB 5,5,8,8-tetramethyl-2-naphtalenyl)propenyl]benzoic acid), a retinoic acid receptor (RAR)-specific agonist, induced apo C-III mRNA in HepG2 cells and primary human hepatocytes. Mutagenesis experiments localized the retinoid responsiveness to a cis-element consisting of two imperfect AGGTCA sequences spaced by one oligonucleotide (DR-1), within the previously identified C3P footprint site. Cotransfection assays showed that RXR, but not RAR, activates apo C-III transcription through this element either as a homo- or as a heterodimer with the peroxisome proliferator-activated receptor. Thus, apo C-III is a target gene for retinoids acting via RXR. Increased apo C-III expression may contribute to the hypertriglyceridemia and atherogenic lipoprotein profile observed after retinoid therapy.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 10/07/20 alle ore 10:50:28