Increased c-Jun N-terminal kinase activation in human endometriotic endothelial cells

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dc.authoridUz, Yesim/0000-0002-0381-4590
dc.contributor.authorUz, Yesim Hulya
dc.contributor.authorMurk, William
dc.contributor.authorBozkurt, Idil
dc.contributor.authorKizilay, Gulnur
dc.contributor.authorArici, Aydin
dc.contributor.authorKayisli, Umit Ali
dc.date.accessioned2024-06-12T11:00:24Z
dc.date.available2024-06-12T11:00:24Z
dc.date.issued2011
dc.departmentTrakya Üniversitesien_US
dc.description.abstractEndometriosis is a common inflammatory gynecological disease characterized by the presence of endometrial tissue outside of the uterine cavity. The c-Jun N-terminal kinase (JNK) is a subfamily of the mitogen-activated protein kinases (MAPKs) involved in cellular processes ranging from cytokine expression to apoptosis, and is activated in response to inflammation and cellular stress. We hypothesized that inflammatory cytokines in the peritoneal microenvironment increase JNK MAPK activity in endometriotic endothelial cells, and that human endometrial endothelial cells (HEECs) may be involved in inflammatory pathogenesis of endometriosis. Thus, we evaluated the expression of the total- and phosphorylated-(phospho)-JNK in endometrial and endometriotic endothelial cells in vivo, and in HEECs treated with normal fperitoneal fluid (NPF), endometriotic peritoneal fluid (EPF), and the inflammatory cytokines interleukin-1beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) in vitro. Phospho-JNK immunoreactivity in HEECs in normal endometrium was significantly higher in the early proliferative and late secretory phases compared to other phases. Both eutopic and ectopic HEECs from the early secretory phase also revealed higher phospho-JNK immunoreactivity, compared to their respective cycle-matched normal HEECs. Moreover, HEECs treated with EPF showed significantly higher phospho-JNK levels compared to that in HEECs treated with NPF. In conclusion, our in vivo and in vitro findings suggest that increased phosphorylation of JNK in HEECs from women with endometriosis is likely due to high level of IL-1 beta and TNF-alpha in peritoneal fluid; this in turn may up-regulate inflammatory cytokine expression and thus play a role in the pathogenesis of endometriosis.en_US
dc.identifier.doi10.1007/s00418-010-0770-2
dc.identifier.endpage91en_US
dc.identifier.issn0948-6143
dc.identifier.issn1432-119X
dc.identifier.issue1en_US
dc.identifier.pmid21170656en_US
dc.identifier.scopus2-s2.0-78651502316en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage83en_US
dc.identifier.urihttps://doi.org/10.1007/s00418-010-0770-2
dc.identifier.urihttps://hdl.handle.net/20.500.14551/20816
dc.identifier.volume135en_US
dc.identifier.wosWOS:000286794000009en_US
dc.identifier.wosqualityQ1en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSpringeren_US
dc.relation.ispartofHistochemistry And Cell Biologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectEndometriosisen_US
dc.subjectMAPKen_US
dc.subjectJNKen_US
dc.subjectHuman Endometrial Endothelial Cellsen_US
dc.subjectCytokinesen_US
dc.subjectMonocyte Chemotactic Protein-1en_US
dc.subjectPeritoneal-Fluiden_US
dc.subjectPotential Mechanismen_US
dc.subjectExpressionen_US
dc.subjectWomenen_US
dc.subjectInterleukin-8en_US
dc.subjectCytokinesen_US
dc.subjectGrowthen_US
dc.subjectSubpopulationsen_US
dc.subjectPathogenesisen_US
dc.titleIncreased c-Jun N-terminal kinase activation in human endometriotic endothelial cellsen_US
dc.typeArticleen_US

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