Overexpression of maternal sFlt1 (Soluble fms-Like Tyrosine Kinase-1) induces dysregulation of galectin-1 at the maternal-fetal interface

Preeclampsia (PE) is a heterogeneous pregnancy syndrome defined by hypertension with or without proteinuria developed after the 20 weeks of gestation. This pregnancy complication is the leading cause of perinatal morbidity and mortality in mothers worldwide. Abnormal placental angiogenesis during gestation resulting from high levels of anti-angiogenic factors, soluble fms-like tyrosine kinase-1 (sFlt1) and soluble endoglin, has been implicated in preeclampsia pathogenesis. Indeed, overexpression of circulating maternal human sFlt1 (hsFlt1) is sufficient to induce preeclampsia-like symptoms in mice. This preeclampsia mouse model is characterized by a shallow trophoblast invasion and impaired spiral artery (SpA)-remodeling. Knowing the key roles played by galectins in the vascular adaptation to pregnancy, we investigate the galectin signature at the maternal-fetal interface in the sFlt1-transgenic mice with systemic hsFlt1 overexpression from mid-gestation onwards. Our analysis revealed up-regulation of placental galectin-1 expression in the decidua and junctional zone layers of the placenta, and to a lesser extent in the giant cell layer derived from hsFlt1 transgenic pregnancies. In contrast, placental galectin-3 and galectin-9 expression showed no significant changes upon hsFLT1 overexpression. Overall, our findings indicate that galectin-1 is sensitive to changes in the anti-angiogenic status caused by abnormal placenta angiogenesis and is consistent with the previously reported role of this lectin on endothelial cell functions.