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dc.contributor.authorDeepak, Venkataraman
dc.contributor.authorSahu, Margaret B.
dc.contributor.authorYu, Jianshi
dc.contributor.authorJones, Jace W.
dc.contributor.authorKane, Maureen A.
dc.contributor.authorTaylor, Robert N.
dc.contributor.authorBadell, Martina L.
dc.contributor.authorSidell, Neil
dc.contributor.authorRajakumar, Augustine
dc.date.accessioned2020-03-05T16:00:01Z
dc.date.available2020-03-05T16:00:01Z
dc.date.issued2019-03-18
dc.identifier.citationDeepak, V., Sahu, M.B., Yu, J., Jones, J.W., Kane, M.A., Taylor, R.N., Badell, M.L., Sidell, N. and Rajakumar, A., (2019). 'Retinoic acid is a negative regulator of sFLT1 expression in decidual stromal cells, and its levels are reduced in preeclamptic decidua'. Hypertension, 73(5), pp. 1104-1111.en_US
dc.identifier.issn0194-911X
dc.identifier.doi10.1161/hypertensionaha.118.12564
dc.identifier.urihttp://hdl.handle.net/10545/624553
dc.description.abstractsFLT1 (soluble VEGF [vascular endothelial growth factor] receptor-1) levels are increased in preeclampsia—a pathological condition of pregnancy. The mechanism of sFLT1 overexpression by gestational tissues, particularly the decidua, remains unknown. Mass spectrometry measurement of the active retinoid metabolite, all-trans retinoic acid (RA), showed significantly lower levels of RA in preeclamptic versus normotensive decidua. In this study, we investigated the involvement of RA in regulating decidual sFLT1 expression. When decidual stromal cells (DSCs) isolated from the decidua basalis of normotensive and preeclampsia placentas were treated with BMS493—a pan-RAR (RA nuclear receptor) antagonist—upregulation of sFLT1 expression was observed. Conversely, treatment with RA resulted in downregulation of sFLT1 in normotensive DSCs and preeclampsia DSCs. Unlike treatment with cAMP, which induces decidualization while downregulating sFLT1, RA treatment did not alter DSC expression of prolactin—a marker of decidualization—or FOXO1 (forkhead box protein 01)—a transcription factor required for prolactin upregulation. TFAP2A (transcription factor AP-2-alpha [activating enhancer-binding protein 2 alpha]), a different transcription factor was upregulated in normotensive DSCs but not in preeclampsia DSCs after RA treatment. Collectively, our data show that RA suppresses sFLT1 expression in DSCs independently of cellular decidualization. These findings suggest that reduced decidual RA levels may contribute to preeclampsia pathogenesis by allowing sFLT1 accumulation at the maternal-fetal interface.en_US
dc.description.sponsorshipKatz Foundationen_US
dc.language.isoenen_US
dc.publisherOvid Technologies (Wolters Kluwer Health)en_US
dc.relation.urlhttps://www.ahajournals.org/doi/full/10.1161/HYPERTENSIONAHA.118.12564en_US
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectsFlt1en_US
dc.subjectPreeclampsiaen_US
dc.subjectRetinoic aciden_US
dc.subjectDecidual cellsen_US
dc.titleRetinoic acid is a negative regulator of sFLT1 expression in decidual stromal cells, and its levels are reduced in preeclamptic deciduaen_US
dc.typeArticleen_US
dc.identifier.eissn1524-4563
dc.contributor.departmentEmory Universityen_US
dc.identifier.journalHypertensionen_US
dc.identifier.pii10.1161/HYPERTENSIONAHA.118.12564
dc.source.journaltitleHypertension
dc.source.volume73
dc.source.issue5
dc.source.beginpage1104
dc.source.endpage1111
dcterms.dateAccepted2019-02-24
dc.author.detail787178en_US


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Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivatives 4.0 International