Publication: 17 beta-estradiol modulates endothelin-1 expression and release in human endothelial cells
dc.contributor.authors | Bilsel, AS; Moini, H; Tetik, E; Aksungar, F; Kaynak, B; Ozer, A | |
dc.date.accessioned | 2022-03-14T10:01:03Z | |
dc.date.available | 2022-03-14T10:01:03Z | |
dc.date.issued | 2000-06 | |
dc.description.abstract | Objective: In this study the role of 17 beta-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 17 beta-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. (C) 2000 Elsevier Science B.V. All rights reserved. | |
dc.identifier.doi | 10.1016/S0008-6363(00)00046-8 | |
dc.identifier.issn | 0008-6363 | |
dc.identifier.pubmed | 10912468 | |
dc.identifier.uri | https://hdl.handle.net/11424/243900 | |
dc.identifier.wos | WOS:000087874500024 | |
dc.language.iso | eng | |
dc.publisher | ELSEVIER SCIENCE BV | |
dc.relation.ispartof | CARDIOVASCULAR RESEARCH | |
dc.rights | info:eu-repo/semantics/openAccess | |
dc.subject | endothelial function | |
dc.subject | endothelins | |
dc.subject | nitric oxide | |
dc.subject | hormones | |
dc.subject | gene expression | |
dc.subject | NITRIC-OXIDE | |
dc.subject | POSTMENOPAUSAL WOMEN | |
dc.subject | CORONARY-ARTERIES | |
dc.subject | ESTROGEN | |
dc.subject | RESPONSES | |
dc.subject | THROMBIN | |
dc.subject | PEPTIDE | |
dc.subject | AORTA | |
dc.subject | INHIBITION | |
dc.subject | MECHANISMS | |
dc.title | 17 beta-estradiol modulates endothelin-1 expression and release in human endothelial cells | |
dc.type | article | |
dspace.entity.type | Publication | |
local.avesis.id | e63aaaaf-1b64-415e-844e-4211a465f7ee | |
local.import.package | SS16 | |
local.indexed.at | WOS | |
local.indexed.at | SCOPUS | |
local.journal.numberofpages | 6 | |
oaire.citation.endPage | 584 | |
oaire.citation.issue | 3 | |
oaire.citation.startPage | 579 | |
oaire.citation.title | CARDIOVASCULAR RESEARCH | |
oaire.citation.volume | 46 |
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