Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Role of ERK MAP kinases in responses of cultured human airway smooth muscle cells to IL-1 beta
Autore:
Laporte, JD; Moore, PE; Abraham, JH; Maksym, GN; Fabry, B; Panettieri, RA; Shore, SA;
Indirizzi:
Harvard Univ, Sch Publ Hlth, Physiol Program, Boston, MA 02115 USA HarvardUniv Boston MA USA 02115 h, Physiol Program, Boston, MA 02115 USA Univ Penn, Sch Med, Dept Med, Div Pulm & Crit Care, Philadelphia, PA 19104USA Univ Penn Philadelphia PA USA 19104 Crit Care, Philadelphia, PA 19104USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
fascicolo: 5, volume: 277, anno: 1999,
pagine: L943 - L951
SICI:
1040-0605(199911)277:5<L943:ROEMKI>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACTIVATED PROTEIN-KINASE; TUMOR-NECROSIS-FACTOR; MITOGEN-INDUCIBLE CYCLOOXYGENASE; SIGNAL-TRANSDUCTION PATHWAYS; BRONCHOALVEOLAR LAVAGE FLUID; PHOSPHOLIPASE A(2); PROSTAGLANDIN E-2; GROWTH-FACTOR; EXPRESSION; INTERLEUKIN-1;
Keywords:
extracellular signal-regulated kinase; mitogen-activated protein; interleukin-1 beta; prostaglandin E-2; beta-adrenergic responses; PD-98059; U-126; magnetic twisting cytometry; cyclooxygenase;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Laporte, JD Harvard Univ, Sch Publ Hlth, Physiol Program, 665 Huntington Ave, Boston, MA 02115 USA Harvard Univ 665 Huntington Ave Boston MA USA 02115 02115 USA
Citazione:
J.D. Laporte et al., "Role of ERK MAP kinases in responses of cultured human airway smooth muscle cells to IL-1 beta", AM J P-LUNG, 277(5), 1999, pp. L943-L951

Abstract

We have previously reported that interleukin (IL)-1 beta causes beta-adrenergic hyporesponsiveness in cultured human airway smooth muscle cells by increasing cyclooxygenase-2 (COX-2) expression and prostanoid formation. The purpose of this study was to determine whether extracellular signal-regulated kinases (ERKs) are involved in these events. Levels of phosphorylated ERK (p42 and p44) increased 8.3- and 18-fold, respectively, 15 min after treatment with IL-1 beta (20 mg/ml) alone. Pretreating cells with the mitogen-activated protein kinase kinase inhibitor PD-98059 or U-126 (2 h before IL-1beta treatment) decreased ERK phosphorylation. IL-1 beta (20 ng/ml for 22 h) alone caused a marked induction of COX-2 and increased basal PGE(2) release 28-fold (P < 0.001). PD-98059 (100 mu M) and U-126 (10 mu M) each decreased COX-2 expression when administered before IL-1 beta treatment. In control cells, PD-98059 and U-126 had no effect on basal or arachidonic acid (AA; 10 mu M)-stimulated PGE(2) release, but both inhibitors caused a significant decrease in bradykinin (BK; 1 mu M)-stimulated PGE(2) release, consistent with a role for ERK in the activation of phospholipase A(2) by BK. In IL-lp-treated cells, prior administration of PD-98059 caused 81, 92 and 40% decreases in basal and BK-and AA-stimulated PGE(2) release, respectively (P< 0.01), whereas administration of PD-98059 20 h after IL-1 beta resulted in only 38 and 43% decreases in basal and BK-stimulated PGE(2) release, respectively (P < 0.02) and had no effect on AA-stimulated PGE(2) release. IL-1 beta attenuated isoproterenol-induced decreases in human airway smooth muscle stiffness as measured by magnetic twisting cytometry, and PD-98059 or U-126 abolished this effect in a concentrationdependent manner. These results are consistent with the hypothesis that ERKs are involved early in the signal transduction pathway through which IL-1 beta induces PGE(2) synthesisand beta-adrenergic hyporesponsiveness and that ERKs act by inducing COX-2and activating phospholipase A(2).

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 24/09/20 alle ore 11:09:40