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dc.contributor.authorGaccioli, Francesca
dc.contributor.authorSovio, Ulla
dc.contributor.authorGong, Sungsam
dc.contributor.authorCook, Emma
dc.contributor.authorCharnock-Jones, D Stephen
dc.contributor.authorSmith, Gordon CS
dc.date.accessioned2022-06-15T23:30:21Z
dc.date.available2022-06-15T23:30:21Z
dc.date.issued2023-02
dc.identifier.issn0194-911X
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/338135
dc.description.abstractBACKGROUND: Preeclampsia and fetal growth restriction (FGR) are both associated with an increased ratio of sFLT1 (soluble fms-like tyrosine kinase-1) to PlGF (placenta growth factor) in maternal serum. In preeclampsia, it is assumed that increased placental release of sFLT1 results in PlGF being bound and inactivated. However, direct evidence for this model is incomplete, and it is unclear whether the same applies in FGR. METHODS: We conducted a prospective cohort study where we followed 4212 women having first pregnancies from their dating ultrasound, obtained blood samples serially through the pregnancy, and performed systematic sampling of the placenta after delivery. The aim of the present study was to determine the relationship between protein levels of sFLT1 and PlGF in maternal serum measured at ≈36 weeks and placental tissue lysates obtained after term delivery in 82 women with preeclampsia, 50 women with FGR, and 132 controls. RESULTS: The sFLT1:PlGF ratio was increased in both preeclampsia and FGR in both the placenta and maternal serum. However, in preeclampsia, the maternal serum ratio of sFLT1:PlGF was strongly associated with placental sFLT1 level (r=0.45; P<0.0001) but not placental PlGF level (r=-0.17; P=0.16). In contrast, in FGR, the maternal serum ratio of sFLT1:PlGF was strongly associated with placental PlGF level (r=-0.35; P=0.02) but not sFLT1 level (r=0.04; P=0.81). CONCLUSIONS: We conclude that the elevated sFLT1:PlGF ratio is primarily driven by increased placental sFLT1 in preeclampsia, whereas in FGR, it is primarily driven by decreased placental PlGF.
dc.description.sponsorshipThe work was supported by the National Institute for Health Research (NIHR) Cambridge Biomedical Research Centre (Women’s Health theme), and grants from the Medical Research Council (United Kingdom; MR/K021133/1), and supported by the NIHR Cambridge Clinical Research Facility.
dc.publisherOvid Technologies (Wolters Kluwer Health)
dc.rightsAll Rights Reserved
dc.rights.urihttp://www.rioxx.net/licenses/all-rights-reserved
dc.titleIncreased Placental sFLT1 (Soluble fms-Like Tyrosine Kinase Receptor-1) Drives the Antiangiogenic Profile of Maternal Serum Preceding Preeclampsia but Not Fetal Growth Restriction.
dc.typeArticle
dc.publisher.departmentDepartment of Obstetrics And Gynaecology
dc.date.updated2022-06-14T10:21:34Z
prism.publicationNameHypertension
dc.identifier.doi10.17863/CAM.85544
dcterms.dateAccepted2022-05-26
rioxxterms.versionofrecord10.1161/HYPERTENSIONAHA.122.19482
rioxxterms.versionAM
dc.contributor.orcidGaccioli, Francesca [0000-0001-7178-8921]
dc.contributor.orcidSovio, Ulla [0000-0002-0799-1105]
dc.contributor.orcidGong, Sungsam [0000-0001-5796-4423]
dc.contributor.orcidCharnock-Jones, D Stephen [0000-0002-2936-4890]
dc.contributor.orcidSmith, Gordon CS [0000-0003-2124-0997]
dc.identifier.eissn1524-4563
rioxxterms.typeJournal Article/Review
pubs.funder-project-idCambridge University Hospitals NHS Foundation Trust (CUH) (146281)
pubs.funder-project-idMedical Research Council (MR/K021133/1)
cam.issuedOnline2022-07-22
cam.orpheus.successWed Aug 03 09:45:51 BST 2022 - Embargo updated
cam.orpheus.counter4
cam.depositDate2022-06-14
pubs.licence-identifierapollo-deposit-licence-2-1
pubs.licence-display-nameApollo Repository Deposit Licence Agreement
rioxxterms.freetoread.startdate2023-01-22


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