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Titolo:
PROSTANOIDS MEDIATE IL-1-BETA-INDUCED BETA-ADRENERGIC HYPORESPONSIVENESS IN HUMAN AIRWAY SMOOTH-MUSCLE CELLS
Autore:
LAPORTE JD; MOORE PE; PANETTIERI RA; MOELLER W; HEYDER J; SHORE SA;
Indirizzi:
HARVARD UNIV,SCH PUBL HLTH,PHYSIOL PROGRAM,665 HUNTINGTON AVE BOSTON MA 02115 UNIV PENN,SCH MED,DEPT MED,DIV PULM & CRIT CARE PHILADELPHIA PA 19002 GSF,NATL RES CTR ENVIRONM OBERSCHLEISSHEIM GERMANY HLTH INST INHALAT BIOL OBERSCHLEISSHEIM GERMANY
Titolo Testata:
American journal of physiology. Lung cellular and molecular physiology
fascicolo: 3, volume: 19, anno: 1998,
pagine: 491 - 501
SICI:
1040-0605(1998)19:3<491:PMIBH>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
DEPENDENT PROTEIN-KINASE; BRONCHOALVEOLAR LAVAGE FLUID; HUMAN ENDOTHELIAL-CELLS; CYCLIC-AMP; BETA-2-ADRENERGIC RECEPTOR; INDUCIBLE CYCLOOXYGENASE; ADENYLYL-CYCLASE; MESSENGER-RNA; PROSTAGLANDIN SYNTHESIS; MOLECULAR MECHANISMS;
Keywords:
PROSTAGLANDIN E-2; CYTOSKELETAL MECHANICS; INDOMETHACIN; NS-398; ADENOSINE 3',5'-CYCLIC MONOPHOSPHATE; INTERLEUKIN-1-BETA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
53
Recensione:
Indirizzi per estratti:
Citazione:
J.D. Laporte et al., "PROSTANOIDS MEDIATE IL-1-BETA-INDUCED BETA-ADRENERGIC HYPORESPONSIVENESS IN HUMAN AIRWAY SMOOTH-MUSCLE CELLS", American journal of physiology. Lung cellular and molecular physiology, 19(3), 1998, pp. 491-501

Abstract

We have previously reported that pretreatment of cultured human airway smooth muscle (HASM) cells with interleukin-1 beta (IL-1 beta) results in decreased beta-adrenergic responsiveness. The purpose of this study was to determine whether prostanoids released as a result of cyclooxygenase-2 (COX-2) induction by IL-1 beta contribute to this effect of the cytokine. Confluent serum-deprived HASM cells were studied in passages 4-7. IL-1 beta (20 ng/ml for 22 h) reduced the ability of the beta-agonist isoproterenol (Iso) to decrease stiffness of HASM: cells as measured by magnetic twisting cytometry. The effect of IL-1 beta on Iso-induced changes in cell stiffness was abolished by nonselective [indomethacin (Indo), 10(-6) M] and selective (NS-398, 10(-5) M) COX-2 inhibitors. Indo and NS-398 also inhibited both the increased basal cAMP and the decreases in Iso-stimulated cAMP production induced by IL-1 beta. IL-1 beta (20 ng/ml for 22 h) caused an increase in both basal (15-fold) and arachidonic acid (AA)-stimulated (10-fold) PGE(2) release. Indo blocked basal and AA-stimulated PGE(2) release in both control and IL-1 beta-treated cells. NS-398 also markedly reduced basal and AA-stimulated PGE(2) release in IL-1 beta-treated cells but had no significant effect on AA-stimulated PGE(2) release in control cells. Western blot analysis confirmed the induction of COX-2 by IL-1 beta. Exogenously administered PGE(2) (10(-7) M, 22 h) caused a significant reduction in the ability of Iso to decrease cell stiffness, mimicking the effects of IL-1 beta. Cycloheximide (10 mu g/ml for 24 h), an inhibitor of protein synthesis, also abolished the effects of IL-1 beta on Iso-induced cell stiffness changes and cAMP formation. In summary, our results indicate that IL-1 beta significantly increases prostanoid release by HASM cells as a result of increased COX-2 expression. The prostanoids appear to contribute to beta-adrenergic hyporesponsiveness, perhapsby heterologous desensitization of the beta(2) receptor.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/04/20 alle ore 03:56:34