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Titolo:
ACTIVATION OF HUMAN AORTIC SMOOTH-MUSCLE CELLS IS INHIBITED BY PPAR-ALPHA BUT NOT BY PPAR-GAMMA ACTIVATORS
Autore:
STAELS B; KOENIG W; HABIB A; MERVAL R; LEBRET M; TORRA IP; DELERIVE P; FADEL A; CHINETTI G; FRUCHART JC; NAJIB J; MACLOUF J; TEDGUI A;
Indirizzi:
INST PASTEUR,DEPT ATHEROSCLEROSE,INSERM,U325,1 RUE CALMETTE F-59019 LILLE FRANCE UNIV LILLE 2,FAC PHARM F-59006 LILLE FRANCE UNIV ULM,DEPT INTERNAL MED CARDIOL 2 D-89081 ULM GERMANY INSERM,U348 F-75745 PARIS 10 FRANCE INSERM,U141 F-75745 PARIS 10 FRANCE IFR CIRCULAT LARIBOISIERE F-75745 PARIS 10 FRANCE
Titolo Testata:
Nature
fascicolo: 6687, volume: 393, anno: 1998,
pagine: 790 - 793
SICI:
0028-0836(1998)393:6687<790:AOHASC>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
FACTOR-KAPPA-B; PHARMACOKINETIC PROPERTIES; THERAPEUTIC USE; EXPRESSION; CYCLOOXYGENASE-2; DYSLIPIDEMIA; SYNTHASE-2; RECEPTOR; ANGINA; SERUM;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
30
Recensione:
Indirizzi per estratti:
Citazione:
B. Staels et al., "ACTIVATION OF HUMAN AORTIC SMOOTH-MUSCLE CELLS IS INHIBITED BY PPAR-ALPHA BUT NOT BY PPAR-GAMMA ACTIVATORS", Nature, 393(6687), 1998, pp. 790-793

Abstract

Peroxisome proliferator-activated receptors (PPARs) are key players in lipid and glucose metabolism and are implicated in metabolic disorders predisposing to atherosclerosis, such as dyslipidaemia and diabetes(1). Whereas PPAR gamma promotes Lipid storage by regulating adipocytedifferentiation, PPAR alpha stimulates the beta-oxidative degradationof fatty acids. PPAR alpha-deficient mice show a prolonged response to inflammatory stimuli, suggesting that PPAR alpha is also a modulatorof inflammation(2). Hypolipidaemic fibrate drugs are PPAR alpha ligands that inhibit the progressive formation of atherosclerotic lesions, which involves chronic inflammatory processes: even in the absence of their atherogenic lipoprotein-lowering effect(4,5). Here we show that PPAR alpha is expressed in human aortic smooth-muscle cells, which participate in plaque formation and post-angioplasty re-stenosis(3). In these smooth-muscle cells, we find that PPAR alpha ligands, and not PPAR gamma ligands, inhibit interleukin-1-induced production of interleukin-6 and prostaglandin and expression of cyclooxygenase-2. This inhibition of cyclooxygenase-2 induction occurs transcriptionally as a result of PPAR alpha repression of NF-kappa B signalling, In hyperlipidaemic patients, fenofibrate treatment decreases the plasma concentrations of interleukin-6, fibrinogen and C-reactive protein. We conclude that activators of PPAR alpha inhibit the inflammatory response of aortic smooth-muscle cells and decrease the concentration of plasma acute-phase proteins, indicating that PPAR alpha in the vascular wall may influence the process of atherosclerosis and re-stenosis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 19:38:08