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dc.contributor.authorAndersson-Rusch, Clara Leticia
dc.contributor.authorLiu, Bin
dc.contributor.authorQuist-Løkken, Ingrid
dc.contributor.authorUpton, Paul D.
dc.contributor.authorOlsen, Oddrun Elise
dc.contributor.authorHella, Hanne
dc.contributor.authorYang, Xudong
dc.contributor.authorTong, Zhen
dc.contributor.authorMorrell, Nicholas W.
dc.contributor.authorHolien, Toril
dc.contributor.authorLi, Wei
dc.description.abstractEndoglin (ENG) is a single-pass transmembrane protein highly expressed on vascular endothelial cells, although low expression levels can be detected in many other cell types. Its extracellular domain can be found in circulation known as soluble endoglin (sENG). Levels of sENG are elevated in many pathological conditions, in particular preeclampsia. We have shown that while loss of cell surface ENG decreases BMP9 signaling in endothelial cells, knocking down ENG in blood cancer cells enhances BMP9 signaling. Despite sENG binding to BMP9 with high affinity and blocking the type II receptor binding site on BMP9, sENG did not inhibit BMP9 signaling in vascular endothelial cells, but the dimeric form of sENG inhibited BMP9 signaling in blood cancer cells. Here we report that in non-endothelial cells such as human multiple myeloma cell lines and the mouse myoblast cell line C2C12, both monomeric and dimeric forms of sENG inhibit BMP9 signaling when present at high concentrations. Such inhibition can be alleviated by the overexpression of ENG and ACVRL1 (encoding ALK1) in the non-endothelial cells. Our findings suggest that the effects of sENG on BMP9 signaling is cell-type specific. This is an important consideration when developing therapies targeting the ENG and ALK1 pathway.en_US
dc.publisherSpringer Natureen_US
dc.rightsNavngivelse 4.0 Internasjonal*
dc.titleHigh concentrations of soluble endoglin can inhibit BMP9 signaling in non-endothelial cellsen_US
dc.title.alternativeHigh concentrations of soluble endoglin can inhibit BMP9 signaling in non-endothelial cellsen_US
dc.typePeer revieweden_US
dc.typeJournal articleen_US
dc.source.journalScientific Reportsen_US

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Navngivelse 4.0 Internasjonal
Except where otherwise noted, this item's license is described as Navngivelse 4.0 Internasjonal