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Article: Oxidative modification enhances lipoprotein(a)-induced overproduction of plasminogen activator inhibitor-1 in cultured vascular endothelial cells

TitleOxidative modification enhances lipoprotein(a)-induced overproduction of plasminogen activator inhibitor-1 in cultured vascular endothelial cells
Authors
Issue Date1997
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/atherosclerosis
Citation
Atherosclerosis, 1997, v. 128 n. 1, p. 1-10 How to Cite?
AbstractElevated levels of plasma lipoprotein (a) [Lp(a)] have been considered as a strong risk factor for premature cardiovascular diseases. Plasminogen activator inhibitor-1 (PAI-1) is the major physiological inhibitor of plasminogen activators (PA). Increases in PAI-1 levels with or without a reduction in PA levels have been frequently found in coronary artery disease patients. The present paper examined the effects of oxidized Lp(a) on the production of PAI-1 in cultured human umbilical vein endothelial cells (HUVEC). Lp(a) and Lp(a)-free, low density lipoprotein (LDL) were prepared using lysine-Sepharose 4B affinity chromatography. Incubations with 10-8 M levels of native Lp(a) moderately increased the levels of biologically active PAI-1 in post-culture medium of HUVEC compared to that with equimolar concentrations of native Lp(a)-free LDL. The release of PAI-1 induced by Lp(a) was enhanced by oxidative modification with copper ion. The stimulation of oxidized Lp(a) on PAI-1 production reached plateau in EC treated with 10-20 nM oxidized Lp(a) modified by 5 μM CuSO4. Treatment with 0.2 μg/ml of actinomycin D significantly reduced native and oxidized Lp(a)-induced PAI-1 overproduction in EC. Increases in the steady state levels of PAI-1 mRNA were detected in native or oxidized Lp(a)-treated EC. The effect of Lp(a)-free oxidized LDL on PAI-1 production was significantly weaker than the equimolar amount of oxidized Lp(a) but stronger than that of native LDL. Treatments with oxidized Lp(a) increased cell-associated PAI-1 to a similar extent as that in native Lp(a)-treated EC. The results of the present paper demonstrate that oxidative modification enhances Lp(a)-induced PAI-1 production in vascular endothelial cells at RNA transcription level, which suggests that oxidization potentially amplifies the anti-fibrinolytic and thrombotic effect of Lp(a).
Persistent Identifierhttp://hdl.handle.net/10722/171203
ISSN
2015 Impact Factor: 3.942
2015 SCImago Journal Rankings: 1.819
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorRen, Sen_US
dc.contributor.authorMan, RYKen_US
dc.contributor.authorAngel, Aen_US
dc.contributor.authorShen, GXen_US
dc.date.accessioned2012-10-30T06:12:41Z-
dc.date.available2012-10-30T06:12:41Z-
dc.date.issued1997en_US
dc.identifier.citationAtherosclerosis, 1997, v. 128 n. 1, p. 1-10en_US
dc.identifier.issn0021-9150en_US
dc.identifier.urihttp://hdl.handle.net/10722/171203-
dc.description.abstractElevated levels of plasma lipoprotein (a) [Lp(a)] have been considered as a strong risk factor for premature cardiovascular diseases. Plasminogen activator inhibitor-1 (PAI-1) is the major physiological inhibitor of plasminogen activators (PA). Increases in PAI-1 levels with or without a reduction in PA levels have been frequently found in coronary artery disease patients. The present paper examined the effects of oxidized Lp(a) on the production of PAI-1 in cultured human umbilical vein endothelial cells (HUVEC). Lp(a) and Lp(a)-free, low density lipoprotein (LDL) were prepared using lysine-Sepharose 4B affinity chromatography. Incubations with 10-8 M levels of native Lp(a) moderately increased the levels of biologically active PAI-1 in post-culture medium of HUVEC compared to that with equimolar concentrations of native Lp(a)-free LDL. The release of PAI-1 induced by Lp(a) was enhanced by oxidative modification with copper ion. The stimulation of oxidized Lp(a) on PAI-1 production reached plateau in EC treated with 10-20 nM oxidized Lp(a) modified by 5 μM CuSO4. Treatment with 0.2 μg/ml of actinomycin D significantly reduced native and oxidized Lp(a)-induced PAI-1 overproduction in EC. Increases in the steady state levels of PAI-1 mRNA were detected in native or oxidized Lp(a)-treated EC. The effect of Lp(a)-free oxidized LDL on PAI-1 production was significantly weaker than the equimolar amount of oxidized Lp(a) but stronger than that of native LDL. Treatments with oxidized Lp(a) increased cell-associated PAI-1 to a similar extent as that in native Lp(a)-treated EC. The results of the present paper demonstrate that oxidative modification enhances Lp(a)-induced PAI-1 production in vascular endothelial cells at RNA transcription level, which suggests that oxidization potentially amplifies the anti-fibrinolytic and thrombotic effect of Lp(a).en_US
dc.languageengen_US
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/atherosclerosisen_US
dc.relation.ispartofAtherosclerosisen_US
dc.rightsAtherosclerosis. Copyright © Elsevier Ireland Ltd.-
dc.subject.meshBlotting, Northernen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCopper Sulfate - Pharmacologyen_US
dc.subject.meshEndothelium, Vascular - Metabolismen_US
dc.subject.meshEnzyme-Linked Immunosorbent Assayen_US
dc.subject.meshHumansen_US
dc.subject.meshLipoprotein(A) - Metabolism - Physiologyen_US
dc.subject.meshOxidation-Reductionen_US
dc.subject.meshPlasminogen Activator Inhibitor 1 - Biosynthesis - Geneticsen_US
dc.subject.meshRna, Messenger - Metabolismen_US
dc.subject.meshThiobarbituric Acid Reactive Substances - Analysisen_US
dc.subject.meshUmbilical Veinsen_US
dc.titleOxidative modification enhances lipoprotein(a)-induced overproduction of plasminogen activator inhibitor-1 in cultured vascular endothelial cellsen_US
dc.typeArticleen_US
dc.identifier.emailMan, RYK:rykman@hkucc.hku.hken_US
dc.identifier.authorityMan, RYK=rp00236en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0021-9150(96)05971-0en_US
dc.identifier.pmid9051192-
dc.identifier.scopuseid_2-s2.0-0031043615en_US
dc.identifier.hkuros25174-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0031043615&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume128en_US
dc.identifier.issue1en_US
dc.identifier.spage1en_US
dc.identifier.epage10en_US
dc.identifier.isiWOS:A1997WG24800001-
dc.publisher.placeIrelanden_US
dc.identifier.scopusauthoridRen, S=7202285617en_US
dc.identifier.scopusauthoridMan, RYK=7004986435en_US
dc.identifier.scopusauthoridAngel, A=7101766569en_US
dc.identifier.scopusauthoridShen, GX=7401966876en_US

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