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 Name:	Freitag, N. and Tirado-González, I. and Barrientos, G. and Herse, F. and Thijssen, V.L.J.L. and Weedon-Fekjær, S.M. and Schulz, H. and Wallukat, G. and Klapp, B.F. and Nevers, T. and Sharma, S. and Staff, A.C. and Dechend, R. and Blois, S.M.
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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