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


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


  • Proceedings of the National Academy of Sciences of the United States of America


  • Proc Natl Acad Sci U S A 110 (28): 11451-11456


  • 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.