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

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...

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Publicado: 2013
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Mus
Acceso en línea:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00278424_v110_n28_p11451_Freitag
http://hdl.handle.net/20.500.12110/paper_00278424_v110_n28_p11451_Freitag
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spelling paper:paper_00278424_v110_n28_p11451_Freitag2023-06-08T14:54:28Z Interfering with Gal-1-mediated angiogenesis contributes to the pathogenesis of preeclampsia galectin 1 lectin messenger RNA vasculotropin receptor 1 vasculotropin receptor 2 angiogenesis animal experiment animal tissue article cell adhesion decidua dendritic cell down regulation female gene expression mouse nonhuman preeclampsia pregnancy priority journal signal transduction Animals Disease Models, Animal Female Galectin 1 Humans Mice Neovascularization, Physiologic Placenta Pre-Eclampsia Pregnancy Trophoblasts Mus 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. 2013 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00278424_v110_n28_p11451_Freitag http://hdl.handle.net/20.500.12110/paper_00278424_v110_n28_p11451_Freitag
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic galectin 1
lectin
messenger RNA
vasculotropin receptor 1
vasculotropin receptor 2
angiogenesis
animal experiment
animal tissue
article
cell adhesion
decidua
dendritic cell
down regulation
female
gene expression
mouse
nonhuman
preeclampsia
pregnancy
priority journal
signal transduction
Animals
Disease Models, Animal
Female
Galectin 1
Humans
Mice
Neovascularization, Physiologic
Placenta
Pre-Eclampsia
Pregnancy
Trophoblasts
Mus
spellingShingle galectin 1
lectin
messenger RNA
vasculotropin receptor 1
vasculotropin receptor 2
angiogenesis
animal experiment
animal tissue
article
cell adhesion
decidua
dendritic cell
down regulation
female
gene expression
mouse
nonhuman
preeclampsia
pregnancy
priority journal
signal transduction
Animals
Disease Models, Animal
Female
Galectin 1
Humans
Mice
Neovascularization, Physiologic
Placenta
Pre-Eclampsia
Pregnancy
Trophoblasts
Mus
Interfering with Gal-1-mediated angiogenesis contributes to the pathogenesis of preeclampsia
topic_facet galectin 1
lectin
messenger RNA
vasculotropin receptor 1
vasculotropin receptor 2
angiogenesis
animal experiment
animal tissue
article
cell adhesion
decidua
dendritic cell
down regulation
female
gene expression
mouse
nonhuman
preeclampsia
pregnancy
priority journal
signal transduction
Animals
Disease Models, Animal
Female
Galectin 1
Humans
Mice
Neovascularization, Physiologic
Placenta
Pre-Eclampsia
Pregnancy
Trophoblasts
Mus
description 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.
title Interfering with Gal-1-mediated angiogenesis contributes to the pathogenesis of preeclampsia
title_short Interfering with Gal-1-mediated angiogenesis contributes to the pathogenesis of preeclampsia
title_full Interfering with Gal-1-mediated angiogenesis contributes to the pathogenesis of preeclampsia
title_fullStr Interfering with Gal-1-mediated angiogenesis contributes to the pathogenesis of preeclampsia
title_full_unstemmed Interfering with Gal-1-mediated angiogenesis contributes to the pathogenesis of preeclampsia
title_sort interfering with gal-1-mediated angiogenesis contributes to the pathogenesis of preeclampsia
publishDate 2013
url https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00278424_v110_n28_p11451_Freitag
http://hdl.handle.net/20.500.12110/paper_00278424_v110_n28_p11451_Freitag
_version_ 1768546664938733568