beta -Adrenergic stimulation induces interleukin-18 expression via beta 2-AR, PI3K, Akt, IKK, and NF- Kappa B
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)- Kappa B. Our results indicate that isoproterenol (...
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Veröffentlicht in: | Biochemical and biophysical research communications 2004-06, Vol.319 (2), p.304-311 |
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creator | Chandrasekar, B Marelli-Berg, F M Tone, M Bysani, S Prabhu, S D Murray, DR |
description | 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)- Kappa B. Our results indicate that isoproterenol (ISO) activates NF- Kappa B DNA binding activity, and induces myocardial and systemic elaboration of IL-18 via beta 2-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 beta 2-AR agonism. Signaling required Gi, PI3K, Akt, IKK, and NF- Kappa B. In conclusion, our results indicate for the first time that isoproterenol induces myocardial and systemic elaboration of IL-18 via a beta 2-AR and NF- Kappa B-dependent mechanism. Similar events may occur in heart failure, a disease state characterized by sustained beta -AR activation. |
doi_str_mv | 10.1016/j.bbrc.2004.04.185 |
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Our results indicate that isoproterenol (ISO) activates NF- Kappa B DNA binding activity, and induces myocardial and systemic elaboration of IL-18 via beta 2-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 beta 2-AR agonism. Signaling required Gi, PI3K, Akt, IKK, and NF- Kappa B. In conclusion, our results indicate for the first time that isoproterenol induces myocardial and systemic elaboration of IL-18 via a beta 2-AR and NF- Kappa B-dependent mechanism. Similar events may occur in heart failure, a disease state characterized by sustained beta -AR activation.</description><identifier>ISSN: 0006-291X</identifier><identifier>DOI: 10.1016/j.bbrc.2004.04.185</identifier><language>eng</language><ispartof>Biochemical and biophysical research communications, 2004-06, Vol.319 (2), p.304-311</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids></links><search><creatorcontrib>Chandrasekar, B</creatorcontrib><creatorcontrib>Marelli-Berg, F M</creatorcontrib><creatorcontrib>Tone, M</creatorcontrib><creatorcontrib>Bysani, S</creatorcontrib><creatorcontrib>Prabhu, S D</creatorcontrib><creatorcontrib>Murray, DR</creatorcontrib><title>beta -Adrenergic stimulation induces interleukin-18 expression via beta 2-AR, PI3K, Akt, IKK, and NF- Kappa B</title><title>Biochemical and biophysical research communications</title><description>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)- Kappa B. Our results indicate that isoproterenol (ISO) activates NF- Kappa B DNA binding activity, and induces myocardial and systemic elaboration of IL-18 via beta 2-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 beta 2-AR agonism. Signaling required Gi, PI3K, Akt, IKK, and NF- Kappa B. In conclusion, our results indicate for the first time that isoproterenol induces myocardial and systemic elaboration of IL-18 via a beta 2-AR and NF- Kappa B-dependent mechanism. 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Our results indicate that isoproterenol (ISO) activates NF- Kappa B DNA binding activity, and induces myocardial and systemic elaboration of IL-18 via beta 2-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 beta 2-AR agonism. Signaling required Gi, PI3K, Akt, IKK, and NF- Kappa B. In conclusion, our results indicate for the first time that isoproterenol induces myocardial and systemic elaboration of IL-18 via a beta 2-AR and NF- Kappa B-dependent mechanism. Similar events may occur in heart failure, a disease state characterized by sustained beta -AR activation.</abstract><doi>10.1016/j.bbrc.2004.04.185</doi><tpages>8</tpages></addata></record> |
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title | beta -Adrenergic stimulation induces interleukin-18 expression via beta 2-AR, PI3K, Akt, IKK, and NF- Kappa B |
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