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dc.contributor.authorSuárez- Martínez, Edu B.
dc.contributor.authorGonzález-Santos, Maryliz
dc.contributor.authorMontealegre, Federico
dc.contributor.authorRuiz, Abigail
dc.contributor.authorSalvo, V. A.
dc.contributor.authorRuiz, Lynnette A.
dc.contributor.authorBáez, P.
dc.date.accessioned2017-06-21T20:12:05Z
dc.date.available2017-06-21T20:12:05Z
dc.date.issued2010-10
dc.identifier.citationRuiz A, Salvo VA, Ruiz LA, Báez P, García M, Flores I. Basal and Steroid Hormone-Regulated Expression of CXCR4 in Human Endometrium and Endometriosis. Reproductive sciences (Thousand Oaks, Calif). 2010;17(10):894-903. doi:10.1177/1933719110379920.en_US
dc.identifier.urihttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4495731/pdf/nihms695819.pdf
dc.identifier.urihttp://hdl.handle.net/11721/1645
dc.description.abstractEndometriosis is associated with activation of local and systemic inflammatory mechanisms, including increased levels of chemokines and other proinflammatory cytokines. We have previously reported increased gene expression of chemokine receptor 4 (CXCR4), the receptor for CXCL12, in lesions of the rat model of endometriosis. The CXCR4-CXCL12 axis has been shown to have both immune (HIV infection, lymphocyte chemotaxis) and nonimmune functions, including roles in tissue repair, angiogenesis, invasion, and migration. There is evidence indicating that these mechanisms are also at play in endometriosis; therefore, we hypothesized that activation of the CXCR4-CXCL12 axis could be responsible, at least in part, for the survival and establishment of endometrial cells ectopically. Immunohistochemistry (IHC) showed that CXCR4 protein levels were significantly higher in endometriotic lesions compared to the endometrium of controls. Next, we determined basal gene and protein expression of CXCR4 and CXCL12 and regulation by estradiol (E2) and/or progesterone (P4) in endometrial cell lines using quantitative polymerase chain reaction (qPCR), and Western blots. Basal CXCR4 gene expression levels were higher in epithelial versus stromal cells; conversely, CXCL12 was expressed at higher levels in stromal vs epithelial cells. CXCR4 gene expression was significantly downregulated by ovarian steroid hormones in endometrial epithelial. These data suggest that steroid modulation of CXCR4 is defective in endometriosis, although the specific mechanism involved remains to be elucidated. These findings have implications for future therapeutic strategies specifically targeting the inflammatory component in endometriosis.en_US
dc.language.isoen_USen_US
dc.publisherSAGE Publicationsen_US
dc.subjectendometriumen_US
dc.subjectendometriosisen_US
dc.subjectchemokinesen_US
dc.subjectCXCR4en_US
dc.subjectCXCL12en_US
dc.subjectovarianen_US
dc.subjectsteroid hormonesen_US
dc.subjectestradiolen_US
dc.subjectprogesteroneen_US
dc.subjectgene expressionen_US
dc.subjectimmunohistochemistryen_US
dc.titleBasal and steroid hormone-regulated expression of CXCR4 in human endometrium and endometriosisen_US
dc.typeArticleen_US
dc.identifier.doidoi:10.1177/1933719110379920en_US
dc.local.DepartmentDepartment of Biologyen_US
dc.local.FacultySelect from the list belowen_US
dc.contributor.campusUniversity of Puerto Rico at Ponce


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