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Article: Insulin-like growth factor I inhibits induction of nitric oxide synthase in vascular smooth muscle cells

TitleInsulin-like growth factor I inhibits induction of nitric oxide synthase in vascular smooth muscle cells
Authors
Issue Date1994
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.org
Citation
Circulation Research, 1994, v. 74 n. 1, p. 24-32 How to Cite?
AbstractExperiments were designed to examine whether or not insulin-like growth factor I (IGF-I), which is produced by vascular cells in response to injury, affects the production of nitric oxide evoked by the inducible nitric oxide synthase in cultures of smooth muscle cells from the rat aorta. Nitric oxide production was assessed indirectly by the measurement of nitrite accumulation and nitric oxide synthase activity by determining the formation of L- citrulline from L-arginine. Nitric oxide synthase was induced in vascular smooth muscle cells that had been exposed to interleukin-1β (IL-1β) or tumor necrosis factor-α (TNF-α). IGF-I inhibited, in a concentration- dependent manner, the production of nitrite and L-citrulline evoked by IL- 1β or TNF-α. The inhibition caused by IGF-I required the presence of the growth factor during the induction of nitric oxide synthase. Two IGF-I- related proteins, IGF-II and insulin, also inhibited, but to a smaller extent, the release of nitrite and the formation of L-citrulline stimulated by IL-1β. Under bioassay conditions, the perfusates from columns containing IL-1β-treated smooth muscle cells relaxed rings of rat aorta without endothelium that had been contracted with phenylephrine; these relaxations were reversed by nitro-L-arginine. Addition of IL-1β-treated vascular smooth muscle cells to indomethacin-treated platelets inhibited their aggregation to thrombin; methylene blue prevented this inhibition. Control smooth muscle cells or cells exposed to IGF-I alone did not have such effects. Smooth muscle cells that had been exposed simultaneously to IL-1β and IGF-I also relaxed detector rat aortic rings, but to a smaller extent, and minimally affected the aggregation, IL-1β caused the expression of inducible nitric oxide synthase mRNA levels in vascular smooth muscle cells; this response was reduced in cells treated with IL-1β in combination with IGF-I. These observations indicate that IGF-I inhibits the cytokine-induced production of nitric oxide by preventing the induction of nitric oxide synthase. They further suggest that IGF-I may be an important modulator of the production of nitric oxide at sites of vascular injury.
Persistent Identifierhttp://hdl.handle.net/10722/171124
ISSN
2015 Impact Factor: 11.551
2015 SCImago Journal Rankings: 5.755
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorSchini, VBen_US
dc.contributor.authorCatovsky, Sen_US
dc.contributor.authorSchrayUtz, Ben_US
dc.contributor.authorBusse, Ren_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:17Z-
dc.date.available2012-10-30T06:12:17Z-
dc.date.issued1994en_US
dc.identifier.citationCirculation Research, 1994, v. 74 n. 1, p. 24-32en_US
dc.identifier.issn0009-7330en_US
dc.identifier.urihttp://hdl.handle.net/10722/171124-
dc.description.abstractExperiments were designed to examine whether or not insulin-like growth factor I (IGF-I), which is produced by vascular cells in response to injury, affects the production of nitric oxide evoked by the inducible nitric oxide synthase in cultures of smooth muscle cells from the rat aorta. Nitric oxide production was assessed indirectly by the measurement of nitrite accumulation and nitric oxide synthase activity by determining the formation of L- citrulline from L-arginine. Nitric oxide synthase was induced in vascular smooth muscle cells that had been exposed to interleukin-1β (IL-1β) or tumor necrosis factor-α (TNF-α). IGF-I inhibited, in a concentration- dependent manner, the production of nitrite and L-citrulline evoked by IL- 1β or TNF-α. The inhibition caused by IGF-I required the presence of the growth factor during the induction of nitric oxide synthase. Two IGF-I- related proteins, IGF-II and insulin, also inhibited, but to a smaller extent, the release of nitrite and the formation of L-citrulline stimulated by IL-1β. Under bioassay conditions, the perfusates from columns containing IL-1β-treated smooth muscle cells relaxed rings of rat aorta without endothelium that had been contracted with phenylephrine; these relaxations were reversed by nitro-L-arginine. Addition of IL-1β-treated vascular smooth muscle cells to indomethacin-treated platelets inhibited their aggregation to thrombin; methylene blue prevented this inhibition. Control smooth muscle cells or cells exposed to IGF-I alone did not have such effects. Smooth muscle cells that had been exposed simultaneously to IL-1β and IGF-I also relaxed detector rat aortic rings, but to a smaller extent, and minimally affected the aggregation, IL-1β caused the expression of inducible nitric oxide synthase mRNA levels in vascular smooth muscle cells; this response was reduced in cells treated with IL-1β in combination with IGF-I. These observations indicate that IGF-I inhibits the cytokine-induced production of nitric oxide by preventing the induction of nitric oxide synthase. They further suggest that IGF-I may be an important modulator of the production of nitric oxide at sites of vascular injury.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.orgen_US
dc.relation.ispartofCirculation Researchen_US
dc.subject.meshAmino Acid Oxidoreductases - Antagonists & Inhibitors - Geneticsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAorta - Cytology - Drug Effects - Enzymologyen_US
dc.subject.meshBiological Assayen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCitrulline - Biosynthesisen_US
dc.subject.meshInsulin-Like Growth Factor I - Pharmacologyen_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 Synthaseen_US
dc.subject.meshPlatelet Aggregationen_US
dc.subject.meshRna, Messenger - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Wistaren_US
dc.subject.meshVasodilationen_US
dc.titleInsulin-like growth factor I inhibits induction of nitric oxide synthase 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.pmid7505207-
dc.identifier.scopuseid_2-s2.0-0028039846en_US
dc.identifier.volume74en_US
dc.identifier.issue1en_US
dc.identifier.spage24en_US
dc.identifier.epage32en_US
dc.identifier.isiWOS:A1994MW25400003-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridSchini, VB=7004113565en_US
dc.identifier.scopusauthoridCatovsky, S=6602617293en_US
dc.identifier.scopusauthoridSchrayUtz, B=6507368561en_US
dc.identifier.scopusauthoridBusse, R=7102661981en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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