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Interfering with Gal-1-mediated angiogenesis contributes to the pathogenesis of preeclampsia

Item Type:Article
Title:Interfering with Gal-1-mediated angiogenesis contributes to the pathogenesis of preeclampsia
Creators: Freitag, N. ORCID logoORCID: https://orcid.org/0000-0001-5972-1863, Tirado-González, I., Barrientos, G., Herse, F. ORCID logoORCID: https://orcid.org/0000-0002-9305-8134, Thijssen, V.L.J.L., Weedon-Fekjær, S.M., Schulz, H. ORCID logoORCID: https://orcid.org/0000-0002-0226-964X, Wallukat, G., Klapp, B.F., Nevers, T., Sharma, S., Staff, A.C., Dechend, R. ORCID logoORCID: https://orcid.org/0000-0001-6636-3080 and Blois, S.M. ORCID logoORCID: https://orcid.org/0000-0002-0434-2660
Abstract:Preeclampsia (PE) is a pregnancy-specific disorder characterized by sudden onset of hypertension and proteinuria in the second half of pregnancy (>20 wk). PE is strongly associated with abnormal placentation and an excessive maternal inflammatory response. Galectin-1 (Gal-1), a member of a family of carbohydrate-binding proteins, has been shown to modulate several processes associated with placentation and to promote maternal tolerance toward fetal antigens. Here, we show that Gal-1 exhibits proangiogenic functions during early stages of pregnancy, promoting decidual vascular expansion through VEGF receptor 2 signaling. Blocking Gal-1-mediated angiogenesis or lectin, galactoside-binding, soluble, 1 deficiency results in a spontaneous PE-like syndrome in mice, mainly by deregulating processes associated with good placentation and maternal spiral artery remodeling. Consistent with these findings, we observed a down-regulation of Gal-1 in patients suffering from early onset PE. Collectively, these results strengthen the notion that Gal-1 is required for healthy gestation and highlight Gal-1 as a valuable biomarker for early PE diagnosis.
Keywords:Animal Disease Models, Galectin 1, Physiologic Neovascularization, Placenta, Pre-Eclampsia, Pregnancy, Trophoblasts, Animals, Mice
Source:Proceedings of the National Academy of Sciences of the United States of America
ISSN:0027-8424
Publisher:National Academy of Sciences
Volume:110
Number:28
Page Range:11451-11456
Date:9 July 2013
Official Publication:https://doi.org/10.1073/pnas.1303707110
PubMed:View item in PubMed

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