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17Beta-estradiol modulates endothelin-1 expression and release in human endothelial cells

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dc.contributor.authorÖZER, SIDIKA AYŞE
dc.contributor.authorsBilsel, A. S.; Moini, H.; Tetik, E.; Aksungar, F.; Kaynak, B.; Ozer, A.
dc.date.accessioned2022-03-15T11:25:04Z
dc.date.available2022-03-15T11:25:04Z
dc.date.issued2000
dc.description.abstractOBJECTIVE: In this study the role of 17beta-estradiol (E2) in the regulation of endothelin-1 (ET-1) mRNA expression and secretion was investigated in cultured human umbilical vein endothelial cells (HUVECs). METHODS: Endothelial cells were either deprived of or treated with 17beta-estradiol (10(-9), 10(-7) M) for 48 h. After the incubation, the effect of E2 on ET-1 gene expression was evaluated by Northern blot analysis. ET-1 release into the media was measured by radioimmunoassay after 6 h of incubation under basal conditions and upon stimulation with thrombin (4 U/ml). In addition, the cyclic guanosine 5'-monophosphate (cGMP) content of cells was assayed by immunoassay. In order to exclude the role of nitric oxide (NO) in E2-induced effects on endothelin-1 gene expression and secretion, nitric oxide synthase (NOS) inhibitor, N-nitro L-arginine methyl ester (1 mM) (L-NAME) was added to the media of some cultures. RESULTS: Incubation of HUVECs with 10(-9) and 10(-7) M E2 for 48 h resulted in a 30 and 47% inhibition of ET-1 mRNA expression, respectively. Incubation with E2 also decreased the basal and thrombin-stimulated ET-1 release while increasing the cGMP content of cells significantly. NOS inhibitor L-NAME increased the release of ET-1 from E2-incubated cells but did not alter the ET-1 release from hormone-deprived cells. However, ET-1 secretion of E2-treated cells were significantly less than the deprived ones. Northern blot analyses also demonstrated that inhibition of NOS only partly attenuated the effect of E2 on ET-1 gene expression. In the presence of L-NAME, treatment with 10(-7) M E2 caused a 12% decrease in ET-1 gene expression. CONCLUSION: The results demonstrate that E2 may play both direct and indirect role in regulation of ET-1 gene expression and production in human endothelial cells. E2-induced increase in NO but decrease in ET-1 production may partly explain the mechanism of the protective effects of the hormone on the cardiovascular system.
dc.identifier.doi10.1016/s0008-6363(00)00046-8
dc.identifier.issn0008-6363
dc.identifier.pubmedPMID: 10912468
dc.identifier.urihttps://hdl.handle.net/11424/250217
dc.language.isoeng
dc.relation.ispartofCardiovascular Research
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectHumans
dc.subjectAnalysis of Variance
dc.subjectCyclic GMP
dc.subjectNitric Oxide
dc.subjectCells, Cultured
dc.subjectEndothelium, Vascular
dc.subjectEstradiol
dc.subjectGene Expression
dc.subjectRNA, Messenger
dc.subjectEndothelin-1
dc.subjectThrombin
dc.subjectBlotting, Northern
dc.subjectStimulation, Chemical
dc.title17Beta-estradiol modulates endothelin-1 expression and release in human endothelial cells
dc.typearticle
dspace.entity.typePublication
local.avesis.ide63aaaaf-1b64-415e-844e-4211a465f7ee
local.import.packageSS23
local.import.sourcePubMed
local.indexed.atPUBMED
oaire.citation.endPage584
oaire.citation.startPage579
oaire.citation.titleCardiovascular Research
oaire.citation.volume3
relation.isAuthorOfPublication8a774c4a-0ff3-45f7-8c72-033222b11f0d
relation.isAuthorOfPublication.latestForDiscovery8a774c4a-0ff3-45f7-8c72-033222b11f0d

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