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Title: | Placental-specific sFLT-1: Role in pre-eclamptic pathophysiology and its translational possibilities for clinical prediction and diagnosis. | Authors: | Tong S.;Kaitu'u-Lino T.J.;Palmer, Kirsten R. | Institution: | (Palmer) Department of Obstetrics and Gynaecology, Monash University, Monash Medical Centre, 246 Clayton Rd, Clayton, VIC 3168, Australia (Palmer, Tong, Kaitu'u-Lino) Translational Obstetric Group, University of Melbourne, Mercy Hospital for Women, 163 Studley Rd, Heidelberg, VIC 3084, Australia | Issue Date: | 3-Jul-2017 | Copyright year: | 2017 | Publisher: | Oxford University Press (E-mail: jnl.info@oup.co.uk) | Place of publication: | United Kingdom | Publication information: | Molecular Human Reproduction. 23 (2) (pp 69-78), 2017. Date of Publication: 06 Feb 2017. | Journal: | Molecular Human Reproduction | Abstract: | Pre-eclampsia is a common obstetric complication globally responsible for a significant burden of maternal and perinatal morbidity and mortality. Central to its pathophysiology is the anti-angiogenic protein, soluble fms-like tyrosine kinase-1 (sFLT-1). sFLT-1 is released from a range of tissues into the circulation, where it antagonizes the activity of vascular endothelial growth factor and placental growth factor leading to endothelial dysfunction. It is this widespread endothelial dysfunction that produces the clinical features of preeclampsia including hypertension and proteinuria. There are multiple splice variants of sFLT-1. One, known as sFLT-1 e15a, evolved quite recently and is only present in humans and higher order primates. This sFLT-1 variant is also the main sFLT-1 secreted from the placenta. Recent work has shown that sFLT-1 e15a is significantly elevated in the placenta and circulation of women with pre-eclampsia. It is also biologically active, capable of causing endothelial dysfunction and the end-organ dysfunction seen in pre-eclampsia. Indeed, the over-expression of sFLT-1 e15a in mice recapitulates the pre-eclamptic phenotype in pregnancy. Therefore, here we propose that sFLT-1 e15a may be the sFLT-1 variant primarily responsible for pre-eclampsia, a uniquely human disease. Furthermore, this placental-specific sFLT-1 variant provides promise for use as an accurate biomarker in the prediction or diagnosis of pre-eclampsia.Copyright © The Author 2016. | DOI: | http://monash.idm.oclc.org/login?url=http://dx.doi.org/10.1093/molehr/gaw077 | Link to associated publication: | Click here for full text options | PubMed URL: | 27986932 [http://www.ncbi.nlm.nih.gov/pubmed/?term=27986932] | ISSN: | 1360-9947 | URI: | https://repository.monashhealth.org/monashhealthjspui/handle/1/38703 | Type: | Review | Subjects: | review messenger RNA/ec [Endogenous Compound] vasculotropin/ec [Endogenous Compound] *vasculotropin receptor 1/ec [Endogenous Compound] *preeclampsia/et [Etiology] clinical practice gene expression gene expression regulation gene overexpression genetic variability human nonhuman pathophysiology *placenta *prediction *preeclampsia/di [Diagnosis] priority journal protein analysis protein expression protein function priority journal protein analysis protein expression protein function Review gene expression gene expression regulation clinical practice gene overexpression genetic variability human nonhuman pathophysiology *placenta *prediction *preeclampsia / *diagnosis / *etiology |
Type of Clinical Study or Trial: | Review article (e.g. literature review, narrative review) |
Appears in Collections: | Articles |
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