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Article: Platelets inhibit the induction of nitric oxide synthesis by interleukin- 1β in vascular smooth muscle cells

TitlePlatelets inhibit the induction of nitric oxide synthesis by interleukin- 1β in vascular smooth muscle cells
Authors
Issue Date1994
PublisherAmerican Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/
Citation
Blood, 1994, v. 83 n. 7, p. 1831-1838 How to Cite?
AbstractWe have investigated the role of platelets in regulating the hemostatic and vasomotor properties of vascular smooth muscle. Experiments were performed to examine the effect of the releasate from activated platelets on the production of nitric oxide from interleukin-1β (IL-1β)-treated cultured rat aortic smooth muscle cells. Treatment of vascular smooth muscle cells with IL-1β resulted in significant accumulation of nitrite in the culture media and in marked elevation of intracellular cyclic guanosine monophosphate (GMP) levels. The releasate from collagen-aggregated platelets blocked the IL-1β-mediated production of nitrite and the accumulation of cyclic GMP in smooth muscle cells in a platelet number-dependent manner. In functional assays, the perfusates from columns containing IL-1β-treated smooth muscle cells relaxed detector blood vessels without endothelium and the addition of IL-1β-treated smooth muscle cells to suspensions of platelets inhibited their thrombin-induced aggregation. The simultaneous treatment of smooth muscle cells with IL-1β and the platelet releasate abolished both the vasorelaxing activities of the perfusates and the inhibition of platelet aggregation. Platelet releasates treated with a neutralizing antibody to platelet-derived growth factor (PDGF) failed to block IL-1β-induced nitric oxide production by the smooth muscle cells, as measured by both biochemical and functional assays. The platelet releasate from a patient with gray platelet syndrome likewise failed to block IL-1β-induced nitrite release by smooth muscle cells. These results demonstrate that platelets downregulate the production of nitric oxide by IL-1β-treated vascular smooth muscle cells through the release of PDGF. This effect may represent a novel mechanism by which platelets regulate vasomotor tone and thrombus formation at sites of vascular injury.
Persistent Identifierhttp://hdl.handle.net/10722/171143
ISSN
2023 Impact Factor: 21.0
2023 SCImago Journal Rankings: 5.272
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorDurante, Wen_US
dc.contributor.authorSchini, VBen_US
dc.contributor.authorKroll, MHen_US
dc.contributor.authorCatovsky, Sen_US
dc.contributor.authorScottBurden, Ten_US
dc.contributor.authorWhite, JGen_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorSchafer, AIen_US
dc.date.accessioned2012-10-30T06:12:23Z-
dc.date.available2012-10-30T06:12:23Z-
dc.date.issued1994en_US
dc.identifier.citationBlood, 1994, v. 83 n. 7, p. 1831-1838en_US
dc.identifier.issn0006-4971en_US
dc.identifier.urihttp://hdl.handle.net/10722/171143-
dc.description.abstractWe have investigated the role of platelets in regulating the hemostatic and vasomotor properties of vascular smooth muscle. Experiments were performed to examine the effect of the releasate from activated platelets on the production of nitric oxide from interleukin-1β (IL-1β)-treated cultured rat aortic smooth muscle cells. Treatment of vascular smooth muscle cells with IL-1β resulted in significant accumulation of nitrite in the culture media and in marked elevation of intracellular cyclic guanosine monophosphate (GMP) levels. The releasate from collagen-aggregated platelets blocked the IL-1β-mediated production of nitrite and the accumulation of cyclic GMP in smooth muscle cells in a platelet number-dependent manner. In functional assays, the perfusates from columns containing IL-1β-treated smooth muscle cells relaxed detector blood vessels without endothelium and the addition of IL-1β-treated smooth muscle cells to suspensions of platelets inhibited their thrombin-induced aggregation. The simultaneous treatment of smooth muscle cells with IL-1β and the platelet releasate abolished both the vasorelaxing activities of the perfusates and the inhibition of platelet aggregation. Platelet releasates treated with a neutralizing antibody to platelet-derived growth factor (PDGF) failed to block IL-1β-induced nitric oxide production by the smooth muscle cells, as measured by both biochemical and functional assays. The platelet releasate from a patient with gray platelet syndrome likewise failed to block IL-1β-induced nitrite release by smooth muscle cells. These results demonstrate that platelets downregulate the production of nitric oxide by IL-1β-treated vascular smooth muscle cells through the release of PDGF. This effect may represent a novel mechanism by which platelets regulate vasomotor tone and thrombus formation at sites of vascular injury.en_US
dc.languageengen_US
dc.publisherAmerican Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/en_US
dc.relation.ispartofBlooden_US
dc.subject.meshAnimalsen_US
dc.subject.meshBlood Platelets - Physiologyen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshHumansen_US
dc.subject.meshInterleukin-1 - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effects - Metabolismen_US
dc.subject.meshNitric Oxide - Biosynthesisen_US
dc.subject.meshNitrites - Metabolismen_US
dc.subject.meshPlatelet-Derived Growth Factor - Physiologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Wistaren_US
dc.subject.meshTransforming Growth Factor Beta - Physiologyen_US
dc.titlePlatelets inhibit the induction of nitric oxide synthesis by interleukin- 1β in vascular smooth muscle cellsen_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.pmid8142651-
dc.identifier.scopuseid_2-s2.0-0028329163en_US
dc.identifier.volume83en_US
dc.identifier.issue7en_US
dc.identifier.spage1831en_US
dc.identifier.epage1838en_US
dc.identifier.isiWOS:A1994NE41100016-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridDurante, W=7006946922en_US
dc.identifier.scopusauthoridSchini, VB=7004113565en_US
dc.identifier.scopusauthoridKroll, MH=7102187905en_US
dc.identifier.scopusauthoridCatovsky, S=6602617293en_US
dc.identifier.scopusauthoridScottBurden, T=7004306459en_US
dc.identifier.scopusauthoridWhite, JG=35497393000en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridSchafer, AI=7202243976en_US
dc.identifier.issnl0006-4971-

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