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Article: Inhibition of cytokine-induced nitric oxide production by transforming growth factor-β1 in human smooth muscle cells

TitleInhibition of cytokine-induced nitric oxide production by transforming growth factor-β1 in human smooth muscle cells
Authors
Issue Date1992
PublisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0022-3751
Citation
Journal Of Physiology, 1992, v. 454, p. 451-465 How to Cite?
Abstract1. Experiments were performed to investigate the effects of human recombinant interleukin-1β on the production of vasoactive substances by human aortic smooth muscle cells in culture. Smooth muscle cells were cultured either on microcarrier beads for bioassay experiments, or in multiwell plates for the determination of nitrite levels. 2. Cells were grown on microcarrier beads, treated with interleukin-1β or vehicle (control) for 24 h, and packed in a column which was perfused with oxygenated Krebs-Ringer solution in the presence of indomethacin. The activity of the perfusates was bioassayed by measuring the changes in tension of a contracted ring of Wistar rat aorta without endothelium, and by evaluating the modulation of thrombin-induced platelet aggregation. 3. Perfusates from interleukin-1β treated cells evoked relaxations of the contracted detector tissues, and microcarrier beads covered with treated cells inhibited thrombin-induced platelet aggregation. Superoxide dismutase enhanced these effects whereas Methylene Blue abolished them. Control cells evoke neither relaxation nor inhibition of platelet aggregation. Interleukin-1β induced a time- and concentration-dependent production of nitrite. Cycloheximide and nitro-L-arginine inhibited the relaxations and the production of nitrite evoked by interleukin-1β treated cells. L-Arginine but not D-arginine overcame the blockade elicited by nitro-L-arginine. Transforming growth factor-β1 reduced the interleukin-1β dependent generation of nitrite by cultured smooth muscle cells and relaxation of contracted bioassay tissues. 4. Interleukin-1β, transforming growth factor-β1, Methylene Blue and L-arginine-related compounds did not induce significant variations of tension of the detector rings. 5. These data demonstrate that the inflammatory and immunological mediator interleukin-1 can stimulate the production of a nitric oxide-like substance(s) in cultured human smooth muscle cells leading to the activation of soluble guanylate cyclase. Liberation of transforming growth factor-β by activated platelets may inhibit these reactions.
Persistent Identifierhttp://hdl.handle.net/10722/171071
ISSN
2015 Impact Factor: 4.731
2015 SCImago Journal Rankings: 2.670
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorJunquero, DCen_US
dc.contributor.authorScottBurden, Ten_US
dc.contributor.authorSchini, VBen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:05Z-
dc.date.available2012-10-30T06:12:05Z-
dc.date.issued1992en_US
dc.identifier.citationJournal Of Physiology, 1992, v. 454, p. 451-465en_US
dc.identifier.issn0022-3751en_US
dc.identifier.urihttp://hdl.handle.net/10722/171071-
dc.description.abstract1. Experiments were performed to investigate the effects of human recombinant interleukin-1β on the production of vasoactive substances by human aortic smooth muscle cells in culture. Smooth muscle cells were cultured either on microcarrier beads for bioassay experiments, or in multiwell plates for the determination of nitrite levels. 2. Cells were grown on microcarrier beads, treated with interleukin-1β or vehicle (control) for 24 h, and packed in a column which was perfused with oxygenated Krebs-Ringer solution in the presence of indomethacin. The activity of the perfusates was bioassayed by measuring the changes in tension of a contracted ring of Wistar rat aorta without endothelium, and by evaluating the modulation of thrombin-induced platelet aggregation. 3. Perfusates from interleukin-1β treated cells evoked relaxations of the contracted detector tissues, and microcarrier beads covered with treated cells inhibited thrombin-induced platelet aggregation. Superoxide dismutase enhanced these effects whereas Methylene Blue abolished them. Control cells evoke neither relaxation nor inhibition of platelet aggregation. Interleukin-1β induced a time- and concentration-dependent production of nitrite. Cycloheximide and nitro-L-arginine inhibited the relaxations and the production of nitrite evoked by interleukin-1β treated cells. L-Arginine but not D-arginine overcame the blockade elicited by nitro-L-arginine. Transforming growth factor-β1 reduced the interleukin-1β dependent generation of nitrite by cultured smooth muscle cells and relaxation of contracted bioassay tissues. 4. Interleukin-1β, transforming growth factor-β1, Methylene Blue and L-arginine-related compounds did not induce significant variations of tension of the detector rings. 5. These data demonstrate that the inflammatory and immunological mediator interleukin-1 can stimulate the production of a nitric oxide-like substance(s) in cultured human smooth muscle cells leading to the activation of soluble guanylate cyclase. Liberation of transforming growth factor-β by activated platelets may inhibit these reactions.en_US
dc.languageengen_US
dc.publisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0022-3751en_US
dc.relation.ispartofJournal of Physiologyen_US
dc.subject.meshAmino Acid Oxidoreductases - Metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAorta, Thoracicen_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 - Cytology - Drug Effects - Enzymologyen_US
dc.subject.meshNitric Oxide - Metabolismen_US
dc.subject.meshNitric Oxide Synthaseen_US
dc.subject.meshPlatelet Aggregation - Drug Effectsen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Wistaren_US
dc.subject.meshRecombinant Proteins - Pharmacologyen_US
dc.subject.meshTransforming Growth Factor Beta - Drug Effectsen_US
dc.titleInhibition of cytokine-induced nitric oxide production by transforming growth factor-β1 in human 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.pmid1282159-
dc.identifier.scopuseid_2-s2.0-0026743165en_US
dc.identifier.volume454en_US
dc.identifier.spage451en_US
dc.identifier.epage465en_US
dc.identifier.isiWOS:A1992JH78600023-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridJunquero, DC=26643025500en_US
dc.identifier.scopusauthoridScottBurden, T=7004306459en_US
dc.identifier.scopusauthoridSchini, VB=7004113565en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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