Effect of homocysteine on nitric oxide production in coronary microvascular endothelial cells

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dc.contributor.authorErol, Ayse
dc.contributor.authorCinar, Mehtap G.
dc.contributor.authorCan, Cenk
dc.contributor.authorMurat, Olukman
dc.contributor.authorUelker, Sibel
dc.contributor.authorKosay, Sezen
dc.date.accessioned2019-10-27T19:37:34Z
dc.date.available2019-10-27T19:37:34Z
dc.date.issued2007
dc.departmentEge Üniversitesien_US
dc.description.abstractHyperhomocysteinemia is widely recognized as an independent risk factor for coronary artery vascular disease, although the underlying mechanisms are not well understood. This study aims to investigate the effect of homocysteine on nitric oxide ( NO) production in coronary microvascular endothelial cells (CMECs) and putative mechanisms mediating this effect. CMECs were isolated on Langendorff system by collagenase perfusion of hearts from male rats and cultured. The effect of homocysteine (0.01 to 1 mM) on basal and stimulated NO production was evaluated by measuring nitrite in the culture media after incubation with or without N-G-nitro-L-arginine methyl ester (L-NAME) ( 1 mM), superoxide dismutase (100 U/mL), or catalase ( 1000 U/mL) for 24 h. Total nitrite was measured using Griess reaction after reduction of nitrate to nitrite with nitrate reductase. Homocysteine did not affect basal nitrite accumulation; however, it significantly increased the nitrite accumulation induced by the calcium ionophore A23187 or interleukin-1 beta only at 1 mM. This effect of homocysteine was significantly inhibited by L-NAME, superoxide dismutase, and catalase. In conclusion, homocysteine increases NO release from stimulated CMECs without affecting basal NO production, which is probably accompanied by increased production of reactive oxygen species. It can be postulated that endothelial cells generate NO in order to minimize the damage caused by homocysteine.en_US
dc.identifier.doi10.1080/10623320701421487en_US
dc.identifier.endpage161en_US
dc.identifier.issn1062-3329
dc.identifier.issue3en_US
dc.identifier.pmid17578710en_US
dc.identifier.scopusqualityN/Aen_US
dc.identifier.startpage157en_US
dc.identifier.urihttps://doi.org/10.1080/10623320701421487
dc.identifier.urihttps://hdl.handle.net/11454/39988
dc.identifier.volume14en_US
dc.identifier.wosWOS:000247729400005en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherTaylor & Francis Incen_US
dc.relation.ispartofEndothelium-Journal of Endothelial Cell Researchen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectatherosclerosisen_US
dc.subjectcell culture/isolationen_US
dc.subjectendothelial functionen_US
dc.subjecthomocysteineen_US
dc.subjectnitric oxideen_US
dc.titleEffect of homocysteine on nitric oxide production in coronary microvascular endothelial cellsen_US
dc.typeArticleen_US

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