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Am J Physiol Heart Circ Physiol 279: H566-H576, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 2, H566-H576, August 2000

Interleukin-1beta , Src- and non-Src tyrosine kinases, and nitric oxide synthase induction in rat aorta in vitro

Yu Gui, Xi-Long Zheng, and Morley D. Hollenberg

Endocrine Research Group, Department of Pharmacology and Therapeutics and Department of Medicine, University of Calgary, Faculty of Medicine, Calgary, Alberta, Canada T2N 4N1

We studied the potential roles for endogenous interleukin-1beta (IL-1beta ) and for several signaling pathways in the spontaneous induction in vitro of inducible nitric oxide synthase (iNOS) in endothelium-denuded rat aorta rings. Added IL-1beta augmented, whereas the IL-1beta receptor antagonist IL-1ra blocked, spontaneous iNOS induction. Furthermore, increases in IL-1beta mRNA preceded those of iNOS mRNA. Mitogen-activated protein kinase kinase and phosphatidyl inositol 3' kinase inhibition did not block iNOS induction, whereas nuclear factor kappa B inhibition did. The sarcoma virus tyrosine kinase (Src) family-selective inhibitor 4-amino-5(4-methylphenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (PP1) blocked the upregulation of IL-1beta mRNA and the subsequent induction of iNOS but not the induction of iNOS stimulated by exogenously added IL-1beta . In contrast, the non-Src inhibitors TP 47/AG 213 and genistein and the tyrosine phosphatase inhibitor vanadate did not affect the spontaneous upregulation of IL-1beta mRNA but blocked both the IL-1beta -mediated and spontaneous induction of iNOS. We conclude that 1) the upregulation of tissue IL-1beta , via a signaling pathway involving a Src family kinase, plays a key role in rat vascular iNOS induction and 2) non-Src tyrosine kinases play roles downstream from IL-1beta for iNOS induction.

inducible nitric oxide synthase; vascular smooth muscle; nuclear factor-kappa B; sarcoma virus tyrosine kinase


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