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

Nancy Freitag, Irene Tirado-Gonzaĺez, Gabriela Barrientos, Florian Herse, Victor L.J.L. Thijssen, Susanne M. Weedon-Fekjær, Herbert Schulz, Gerd Wallukat, Burghard F. Klapp, Tania Nevers, Surendra Sharma, Anne Cathrine Staff, Ralf Dechend, Sandra M. Blois

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish (US)
Pages (from-to)11451-11456
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number28
StatePublished - Jul 9 2013
Externally publishedYes

ASJC Scopus subject areas

  • General


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