Regulation of interleukin-1-beta-stimulated inducible nitric oxide synthase expression in cultured vascular smooth muscle cells by hemostatic proteins

Biochemical Pharmacology
W DuranteA I Schafer

Abstract

Experiments were performed to examine the mechanism by which specific hemostatic proteins regulate the release of nitric oxide (NO) from interleukin-1 beta (IL-1beta) stimulated cultured rate aortic smooth muscle cells. Treatment of smooth muscle cells with IL-Beta stimulated inducible nitric oxide synthase (iNOS) mRNA expression, which preceded the release of NO (as measured by the accumulation of nitrite in the culture media). The cytokine-stimulated production of nitrite was blocked by the protein synthesis inhibitor cycloheximide, the transcriptional inhibitor actinomycin D, and the competitive inhibitor of NOS nitro-L-arginine. However, only actinomycin D inhibited IL-1beta-stimulated iNOS mRNA expression, Treatment of smooth muscle cells with IL-1beta in the presence of platelet derived growth factor or thrombin resulted in the inhibition of cytokine-stimulated expression of iNOS mRNA and NO release. The inhibitory effect of thrombin was reversed by hirudin and was mimicked by a 14 amino acid thrombin receptor activating peptide. In contract, the concomitant exposure of smooth muscle cells to IL-1beta-and plasmin resulted resulted in the potentiation of both IL-1beta-stimulated iNOS expression and NO generation. Finally, ...Continue Reading

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Citations

Jan 24, 1998·Biochemical and Biophysical Research Communications·A Krop-WatorekH Nakazato
May 1, 1997·Disease-a-month : DM·R G KilbournC Szabó
Dec 30, 1999·Progress in Retinal and Eye Research·N A Rao, G S Wu
Dec 19, 2000·Biochemical and Biophysical Research Communications·D A TulisA I Schafer
Jan 13, 2004·Journal of Cardiovascular Pharmacology·Loren W KlineChristina G Benishin
Dec 18, 2001·American Journal of Physiology. Cell Physiology·Xingwu TengJohn D Catravas

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