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Titolo:
Post-transcriptional regulation of bradykinin b1 and b2 receptor gene expression in human lung fibroblasts by tumor necrosis factor-alpha: Modulationby dexamethasone
Autore:
Haddad, EB; Fox, AJ; Rousell, J; Burgess, G; McIntyre, P; Barnes, PJ; Chung, KF;
Indirizzi:
Imperial Coll Sch Med, Natl Heart & Lung Inst, Dept Thorac Med, London, England Imperial Coll Sch Med London England , Dept Thorac Med, London, England Novartis Inst Med Sci, London, England Novartis Inst Med Sci London England rtis Inst Med Sci, London, England
Titolo Testata:
MOLECULAR PHARMACOLOGY
fascicolo: 6, volume: 57, anno: 2000,
pagine: 1123 - 1131
SICI:
0026-895X(200006)57:6<1123:PROBBA>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACTIVATED PROTEIN-KINASE; ARTERIAL SMOOTH-MUSCLE; KININ B-1 RECEPTORS; A+U-RICH ELEMENTS; MUSCARINIC RECEPTOR; DOWN-REGULATION; GINGIVAL FIBROBLASTS; UP-REGULATION; GROWTH-FACTOR; MAP KINASE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Haddad, EB Aventis Pharmaceut, Dept Pharmacol, Rainham Rd S, Dagenham RM107XS, Essex, England Aventis Pharmaceut Rainham Rd S Dagenham Essex EnglandRM10 7XS
Citazione:
E.B. Haddad et al., "Post-transcriptional regulation of bradykinin b1 and b2 receptor gene expression in human lung fibroblasts by tumor necrosis factor-alpha: Modulationby dexamethasone", MOLEC PHARM, 57(6), 2000, pp. 1123-1131

Abstract

The cellular and molecular mechanisms governing bradykinin B1 and B2 receptor expression and function are poorly understood. We investigated the regulation of both B1 and B2 receptors in human embryonic lung fibroblasts (HEL299) by the proinflammatory cytokines tumor necrosis factor alpha (TNF-alpha) and interleukin 1 beta (IL-1 beta). TNF-alpha and IL-1 beta both induced a rapid and transient increase in B1 and B2 receptor mRNA expression thatwas maximal by 2 h, accompanied by an increase in B1 and B2 receptor protein, as measured by radioligand binding assay with [H-3]des-Arg(10)-kallidin, and [H-3]bradykinin, respectively. The induced B1 receptors were functionally coupled, because the B1 agonist, des-Arg(10)-kallidin, induced an increase in arachidonic acid release in TNF-alpha-stimulated cells but not in control cells. The induction of B1 and the up-regulation of B2 receptors by TNF-alpha was partly mediated through activation of p38 mitogen-activated protein kinase and that of B2 receptor by protein kinase A. TNF-alpha and IL-1 beta regulation of both B1 and B2 receptors was inhibited by dexamethasone. When compared with vehicle-treated cells, dexamethasone increased the rate of decline of both B1 and B2 receptor mRNAs. Nuclear run-on experimentsdemonstrate that the induction of B1 and the up-regulation of B2 receptorsas well as the inhibitory effect of dexamethasone are entirely mediated through post-transcriptional mechanisms.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 13:53:30