Role of apoptosis, bcl-2 and bax protein expression in premature rupture of fetal membranes

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dc.contributor.authorSagol, S
dc.contributor.authorSagol, O
dc.contributor.authorOzkal, S
dc.contributor.authorAsena, U
dc.date.accessioned2019-10-27T18:43:28Z
dc.date.available2019-10-27T18:43:28Z
dc.date.issued2002
dc.departmentEge Üniversitesien_US
dc.description.abstractOBJECTIVE: To examine the degree of apoptosis in human fetal membranes associated with premature rupture Of membranes (PROM) as compared with normal pregnancies and to evaluate the expression of proapoptotic bax and antiapoptotic bcl-2 gene products. STUDY DESIGN: Fetal membranes from 50 pregnancies were included in the study. Thirty of 50 pregnancies had PROM. Twenty pregnancies with intact membranes served as controls. Chorioamniotic membrane biopsies were taken from the rupture site of the membrane and periphery of the rupture side. In the control group, membrane biopsies were taken from the artificial rupture site, cervical pole of the membranes and, membranes close to the edge of the placenta. In recognizing apoptotic figures, routinely processed samples were stained with hematoxylin and eosin for light microscopic evaluation. Quantification of the apoptotic cells was performed with high-power fields and expressed as the number per 100 cells. The membranes of both groups were then stained with bcl-2 and bax antibodies by using the standard steptavidin-biotin-immunoperoxidase method. Staining with both antibodies were compared between two groups. RESULTS: Apoptotic cells were detected in the amniotic epithelium, in chorionic cells and fibroblastic layer of the fetal membranes. Apoptotic cells were found mostly in the chorionic cells. There was a statistically significant difference between the apoptotic index in PROM and the control group in both rupture and peripheral sites (P<.05), although within each group peripheral and rupture sites showed no difference in terms of apoptotic cell counts. Both bax and bcl-2 expression was observed in 40% of control cases and in 57% and 50% of cases with PROM, respectively, mostly in the chorionic trophoblastic cells. The PROM and control groups showed no statistically significant difference in terms of bcl-2 and bax protein expression. CONCLUSION: Apoptosis may play a role in the pathogenesis of PROM, but the changes in apoptosis do not seem to be mediated by bcl-2 and bax genes in the amniotic membrane. Other regulatory mechanisms must be investigated.en_US
dc.identifier.endpage815en_US
dc.identifier.issn0024-7758
dc.identifier.issn1943-3565
dc.identifier.issue10en_US
dc.identifier.pmid12418062en_US
dc.identifier.scopusqualityQ4en_US
dc.identifier.startpage809en_US
dc.identifier.urihttps://hdl.handle.net/11454/37220
dc.identifier.volume47en_US
dc.identifier.wosWOS:000178826800002en_US
dc.identifier.wosqualityN/Aen_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSci Printers & Publ Incen_US
dc.relation.ispartofJournal of Reproductive Medicineen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectfetal membranesen_US
dc.subjectpremature ruptureen_US
dc.subjectapoptosisen_US
dc.subjectbcl-2 genesen_US
dc.subjectbaxen_US
dc.titleRole of apoptosis, bcl-2 and bax protein expression in premature rupture of fetal membranesen_US
dc.typeArticleen_US

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