GnRH agonist decreases endothelial nitric oxide synthase (eNOS) expression in leiomyoma

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dc.contributor.authorGokdeniz, R
dc.contributor.authorOzen, S
dc.contributor.authorMizrak, B
dc.contributor.authorBazoglu, N
dc.date.accessioned2024-08-04T20:12:10Z
dc.date.available2024-08-04T20:12:10Z
dc.date.issued2000
dc.departmentİnönü Üniversitesien_US
dc.description.abstractObjective: To define the effect of GnRH agonist (GnRHa) treatment on endothelial nitric oxide synthase (eNOS) expression in leiomyoma. As eNOS expression is more pronounced in leiomyoma compared to parental myometrium, we hypothesized that the mechanism(s) of tumor shrinkage by GnRHa may be due to decreased nitric oxide (NO) production in leiomyoma. Methods: Eleven patients with leiomyoma ware operated for myoma enucleation by laparatomy. Six of them were treated with GnRHa every 28 days, three times before the operation. The remaining five patients who had no treatment prior to operation formed the control group. flood was drawn from the patients before treatment and on the day of operation for the assay of serum estradiol (E-2). Immunohistochemical localization of eNOS expression in leiomyoma and myometrium in treated patients, and in leiomyoma in the control group, was performed using monoclonal antibodies specific to eNOS. Results: All treated subjects showed a significant reduction of fibroid volume at the end of therapy. eNOS-positive cells were localized primarily within the vascular endothelium and smooth muscle cells, but had weak expression in fibroid and myometrial muscle cells in the treated group. The immunoreactivity was similar for both the leiomyoma and myometrium (P > 0.05). In contrast to this, the control group had shown strong expression in leiomyoma muscle cells (P < 0.005) in addition to the vascular endothelium and smooth muscle cells. Conclusion: GnRHa-induced tumor shrinkage should be due to diminished eNOS expression, most probably by lowering estrogen secretion. (C) 2000 International Federation of Gynecology and Obstetrics.en_US
dc.identifier.doi10.1016/S0020-7292(00)00198-3
dc.identifier.endpage352en_US
dc.identifier.issn0020-7292
dc.identifier.issue3en_US
dc.identifier.pmid10967169en_US
dc.identifier.scopus2-s2.0-0034283905en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage347en_US
dc.identifier.urihttps://doi.org/10.1016/S0020-7292(00)00198-3
dc.identifier.urihttps://hdl.handle.net/11616/93264
dc.identifier.volume70en_US
dc.identifier.wosWOS:000089324100006en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherElsevier Sci Ireland Ltden_US
dc.relation.ispartofInternational Journal of Gynecology & Obstetricsen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectGnRHaen_US
dc.subjectleiomyomaen_US
dc.subjectimmunohistochemistryen_US
dc.subjectnitric oxideen_US
dc.titleGnRH agonist decreases endothelial nitric oxide synthase (eNOS) expression in leiomyomaen_US
dc.typeArticleen_US

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