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Article: Regulation of smooth muscle cell growth by endothelium-derived factors

TitleRegulation of smooth muscle cell growth by endothelium-derived factors
Authors
Issue Date1994
Citation
Texas Heart Institute Journal, 1994, v. 21 n. 1, p. 91-97 How to Cite?
AbstractThe endothelium is a source of molecules that either stimulate or inhibit the proliferation of the underlying smooth muscle cells. In the normal, healthy vessel wall the smooth muscle cells are quiescent, but they proliferative when damage to the endothelium occurs. The implication of such observations is that although the endothelium provides a source of growth factors, their stimulatory activity on smooth muscle cells is countered by endothelium-derived growth inhibitors. The inhibitors appear to comprise at least 3 distinct types of molecules: heparin/heparan sulfate; transforming growth factor β; and nitric oxide. Each molecule inhibits growth of cultured smooth muscle cells by mechanisms that remain to be elucidated and are discussed in this communication. Heparin/heparan sulfate is the most thoroughly characterized of the 3, and has been used for clinical intervention to prevent restenosis. Transforming growth factor β exhibits bimodal activity on growth, acting as a stimulant at low levels and as an inhibitor at elevated concentrations. Nitric oxide mediated vasorelaxation is dependent upon activation of soluble guanylate cyclase. Because elevation of cyclic guanosine monophosphate in smooth muscle cells depresses their proliferation, nitric oxide would appear to possess the properties necessary to inhibit vascular smooth muscle cell proliferation.
Persistent Identifierhttp://hdl.handle.net/10722/171138
ISSN
2014 Impact Factor: 0.649
2015 SCImago Journal Rankings: 0.343
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorScottBurden, Ten_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:21Z-
dc.date.available2012-10-30T06:12:21Z-
dc.date.issued1994en_US
dc.identifier.citationTexas Heart Institute Journal, 1994, v. 21 n. 1, p. 91-97en_US
dc.identifier.issn0730-2347en_US
dc.identifier.urihttp://hdl.handle.net/10722/171138-
dc.description.abstractThe endothelium is a source of molecules that either stimulate or inhibit the proliferation of the underlying smooth muscle cells. In the normal, healthy vessel wall the smooth muscle cells are quiescent, but they proliferative when damage to the endothelium occurs. The implication of such observations is that although the endothelium provides a source of growth factors, their stimulatory activity on smooth muscle cells is countered by endothelium-derived growth inhibitors. The inhibitors appear to comprise at least 3 distinct types of molecules: heparin/heparan sulfate; transforming growth factor β; and nitric oxide. Each molecule inhibits growth of cultured smooth muscle cells by mechanisms that remain to be elucidated and are discussed in this communication. Heparin/heparan sulfate is the most thoroughly characterized of the 3, and has been used for clinical intervention to prevent restenosis. Transforming growth factor β exhibits bimodal activity on growth, acting as a stimulant at low levels and as an inhibitor at elevated concentrations. Nitric oxide mediated vasorelaxation is dependent upon activation of soluble guanylate cyclase. Because elevation of cyclic guanosine monophosphate in smooth muscle cells depresses their proliferation, nitric oxide would appear to possess the properties necessary to inhibit vascular smooth muscle cell proliferation.en_US
dc.languageengen_US
dc.relation.ispartofTexas Heart Institute Journalen_US
dc.subject.meshAnimalsen_US
dc.subject.meshEndothelial Growth Factors - Physiologyen_US
dc.subject.meshHeparin - Physiologyen_US
dc.subject.meshHeparitin Sulfate - Physiologyen_US
dc.subject.meshMuscle, Smooth, Vascular - Cytologyen_US
dc.subject.meshNitric Oxide - Physiologyen_US
dc.subject.meshTransforming Growth Factor Beta - Physiologyen_US
dc.titleRegulation of smooth muscle cell growth by endothelium-derived factorsen_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.pmid8180516-
dc.identifier.scopuseid_2-s2.0-0028208645en_US
dc.identifier.volume21en_US
dc.identifier.issue1en_US
dc.identifier.spage91en_US
dc.identifier.epage97en_US
dc.identifier.isiWOS:A1994ND56600014-
dc.identifier.scopusauthoridScottBurden, T=7004306459en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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