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Your search keyword '"Murray, David R."' showing total 5 results
Start Over Author "Murray, David R." Publisher elsevier
5 results on '"Murray, David R."'

1. Contributors

Author

ASHFORD, ANNE E., primary, BHALLA, PREM L., additional, CAVANAGH, A.K., additional, DALLING, MICHAEL J., additional, DOMAN, DIANE C., additional, GUBLER, FRANK, additional, MURRAY, DAVID R., additional, Ross, J.D., additional, SIMON, E.W., additional, TRAN, V.N., additional, and TRELEASE, RICHARD N., additional

Published
1984
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4. Beta-adrenergic stimulation induces interleukin-18 expression via beta2-AR, PI3K, Akt, IKK, and NF-kappaB.

Author

Chandrasekar B, Marelli-Berg FM, Tone M, Bysani S, Prabhu SD, and Murray DR

Subjects
Animals, Cells, Cultured, Gene Expression Regulation physiology, I-kappa B Kinase, Male, Mice, Mice, Inbred C57BL, Myocardium cytology, Myocardium enzymology, Promoter Regions, Genetic, Proto-Oncogene Proteins c-akt, Adrenergic beta-Agonists pharmacology, Gene Expression Regulation drug effects, Interleukin-18 genetics, Isoproterenol pharmacology, Myocardium metabolism, NF-kappa B metabolism, Phosphatidylinositol 3-Kinases metabolism, Protein Serine-Threonine Kinases metabolism, Proto-Oncogene Proteins metabolism, Receptors, Adrenergic, beta-2 metabolism
Abstract

We investigated whether beta-adrenergic receptor (beta-AR) stimulation induces the expression of interleukin (IL)-18, a proinflammatory cytokine, in myocardium and in cardiac-derived endothelial cells (CDEC) via activation of nuclear factor (NF)-kappaB. Our results indicate that isoproterenol (ISO) activates NF-kappaB DNA binding activity, and induces myocardial and systemic elaboration of IL-18 via beta2-AR signaling. Furthermore, in CDEC, ISO increased basal and inducible promoter activities, increased IL-18 gene transcription and mRNA stability, and induced IL-18 expression via beta2-AR agonism. Signaling required GiPI3K, PI3K, Akt, IKK, and NF-kappaB. In conclusion, our results indicate for the first time that isoproterenol induces myocardial and systemic elaboration of IL-18 via a beta2-AR and NF-kappaB-dependent mechanism. Similar events may occur in heart failure, a disease state characterized by sustained beta-AR activation.

Published
2004
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