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

TitleRegulation of interleukin-1β-stimulated inducible nitric oxide synthase expression in cultured vascular smooth muscle cells by hemostatic proteins
Authors
Issue Date1996
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/biochempharm
Citation
Biochemical Pharmacology, 1996, v. 51 n. 6, p. 847-853 How to Cite?
AbstractExperiments were performed to examine the mechanism by which specific hemostatic proteins regulate the release of nitric oxide from interleukin-1β (IL-1β) stimulated cultured rat aortic smooth muscle cells. Treatment of smooth muscle cells with IL-β 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-1β-stimulated iNOS mRNA expression. Treatment of smooth muscle cells with IL-1β 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 contrast, the concomitant exposure of smooth muscle cells to IL-1β and plasmin resulted in the potentiation of both IL-1β-stimulated iNOS expression and NO generation. Finally, treatment of smooth muscle cells with IL-1β in the presence of the hemostatic proteins did not affect the half-life of iNOS mRNA. These results demonstrate that specific protein components of the hemostatic system regulate IL-1β-stimulated iNOS mRNA expression in vascular smooth muscle cells. The capacity of hemostatic proteins to modulate the induction of vascular iNOS activity may play an important role in governing the release of NO and regulating thrombogenesis in vivo.
Persistent Identifierhttp://hdl.handle.net/10722/171181
ISSN
2015 Impact Factor: 5.091
2015 SCImago Journal Rankings: 2.263
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorDurante, Wen_US
dc.contributor.authorKroll, MHen_US
dc.contributor.authorOrloff, GJen_US
dc.contributor.authorCunningham, JMen_US
dc.contributor.authorScottBurden, Ten_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorSchafer, AIen_US
dc.date.accessioned2012-10-30T06:12:33Z-
dc.date.available2012-10-30T06:12:33Z-
dc.date.issued1996en_US
dc.identifier.citationBiochemical Pharmacology, 1996, v. 51 n. 6, p. 847-853en_US
dc.identifier.issn0006-2952en_US
dc.identifier.urihttp://hdl.handle.net/10722/171181-
dc.description.abstractExperiments were performed to examine the mechanism by which specific hemostatic proteins regulate the release of nitric oxide from interleukin-1β (IL-1β) stimulated cultured rat aortic smooth muscle cells. Treatment of smooth muscle cells with IL-β 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-1β-stimulated iNOS mRNA expression. Treatment of smooth muscle cells with IL-1β 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 contrast, the concomitant exposure of smooth muscle cells to IL-1β and plasmin resulted in the potentiation of both IL-1β-stimulated iNOS expression and NO generation. Finally, treatment of smooth muscle cells with IL-1β in the presence of the hemostatic proteins did not affect the half-life of iNOS mRNA. These results demonstrate that specific protein components of the hemostatic system regulate IL-1β-stimulated iNOS mRNA expression in vascular smooth muscle cells. The capacity of hemostatic proteins to modulate the induction of vascular iNOS activity may play an important role in governing the release of NO and regulating thrombogenesis in vivo.en_US
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/biochempharmen_US
dc.relation.ispartofBiochemical Pharmacologyen_US
dc.subject.meshAmino Acid Sequenceen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAorta, Thoracic - Drug Effects - Enzymologyen_US
dc.subject.meshCattleen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshEnzyme Induction - Drug Effectsen_US
dc.subject.meshFibrinolysin - Pharmacologyen_US
dc.subject.meshHemostasis - Physiologyen_US
dc.subject.meshInterleukin-1 - Pharmacologyen_US
dc.subject.meshKineticsen_US
dc.subject.meshMolecular Sequence Dataen_US
dc.subject.meshMuscle Proteins - Physiologyen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effects - Enzymologyen_US
dc.subject.meshNitric Oxide Synthase - Biosynthesisen_US
dc.subject.meshNitrites - Metabolismen_US
dc.subject.meshPeptide Fragments - Pharmacologyen_US
dc.subject.meshPlatelet-Derived Growth Factor - Pharmacologyen_US
dc.subject.meshRna, Messenger - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshStimulation, Chemicalen_US
dc.titleRegulation of interleukin-1β-stimulated inducible nitric oxide synthase expression in cultured vascular smooth muscle cells by hemostatic proteinsen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/0006-2952(95)02409-3en_US
dc.identifier.pmid8602881-
dc.identifier.scopuseid_2-s2.0-0029961654en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0029961654&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume51en_US
dc.identifier.issue6en_US
dc.identifier.spage847en_US
dc.identifier.epage853en_US
dc.identifier.isiWOS:A1996TZ10700016-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridDurante, W=7006946922en_US
dc.identifier.scopusauthoridKroll, MH=7102187905en_US
dc.identifier.scopusauthoridOrloff, GJ=36942345100en_US
dc.identifier.scopusauthoridCunningham, JM=7402342358en_US
dc.identifier.scopusauthoridScottBurden, T=7004306459en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridSchafer, AI=7202243976en_US

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