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http://purl.uniprot.org/citations/28633389http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/28633389http://www.w3.org/2000/01/rdf-schema#comment"

Context

Preeclampsia (PE) can be classified into early-onset (<34 weeks of gestation) and late-onset (>34 weeks of gestation) subtypes. Soluble endoglin, an auxiliary receptor for transforming growth factor (TGF)-β ligands, is increased in PE circulation and believed to inhibit TGF-β action by sequestering the ligands. However, soluble endoglin, with a low affinity to TGF-β ligands, has been demonstrated to have little effect by itself on TGF-β action.

Objectives

We examined whether multiple soluble TGF-β receptors are elevated in PE circulation and whether they synergistically block TGF-β signaling.

Design

TGF-β receptors were measured using enzyme-linked immunosorbent assay in sera collected from preeclamptic pregnancies and gestation-age-matched controls. TGF-β signaling was assessed using an in vitro bioassay and a tube formation assay.

Results

TGF-β type I, II, and III receptors were all identified in pregnant serum; all were substantially elevated in early-onset but not late-onset PE. Endoglin was increased in both subtypes. At the greatest concentrations detected in PE, none of these soluble TGF-β receptors alone, including endoglin, inhibited TGF-β signaling. However, when all four soluble receptors were present, signaling of both TGF-β1 and TGF-β2 was substantially reduced. Removal of any one of these soluble receptors alleviated TGF-β1 inhibition; however, removal of soluble TGFβRIII was necessary to relieve TGF-β2 inhibition.

Conclusions

Multiple soluble TGF-β receptors are present in pregnant circulation and elevated in early-onset PE; they synergistically inhibit TGF-β signaling, which might be more likely to occur in early-onset than late-onset PE. Reducing soluble TGFβRIII, rather than endoglin, would be more effective in alleviating the inhibition of both TGF-β1 and TGF-β2 signaling in PE."xsd:string
http://purl.uniprot.org/citations/28633389http://purl.org/dc/terms/identifier"doi:10.1210/jc.2017-01150"xsd:string
http://purl.uniprot.org/citations/28633389http://purl.uniprot.org/core/author"Chen Q."xsd:string
http://purl.uniprot.org/citations/28633389http://purl.uniprot.org/core/author"Wang Y."xsd:string
http://purl.uniprot.org/citations/28633389http://purl.uniprot.org/core/author"Zhao M."xsd:string
http://purl.uniprot.org/citations/28633389http://purl.uniprot.org/core/author"Walton K."xsd:string
http://purl.uniprot.org/citations/28633389http://purl.uniprot.org/core/author"Harrison C."xsd:string
http://purl.uniprot.org/citations/28633389http://purl.uniprot.org/core/author"Nie G."xsd:string
http://purl.uniprot.org/citations/28633389http://purl.uniprot.org/core/date"2017"xsd:gYear
http://purl.uniprot.org/citations/28633389http://purl.uniprot.org/core/name"J Clin Endocrinol Metab"xsd:string
http://purl.uniprot.org/citations/28633389http://purl.uniprot.org/core/pages"3065-3074"xsd:string
http://purl.uniprot.org/citations/28633389http://purl.uniprot.org/core/title"Multiple Soluble TGF-beta Receptors in Addition to Soluble Endoglin Are Elevated in Preeclamptic Serum and They Synergistically Inhibit TGF-beta Signaling."xsd:string
http://purl.uniprot.org/citations/28633389http://purl.uniprot.org/core/volume"102"xsd:string
http://purl.uniprot.org/citations/28633389http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/28633389
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