Decrypting intracellular galectin-1 networks in healthy and diseased pregnancy

• Applicant: Professorin Dr. Sandra Maria Blois
• Subject Area: Gynaecology and Obstetrics ; Reproductive Medicine, Urology
• Term: since 2018
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 397472343

Preeclampsia (PE) is a heterogeneous syndrome and leading cause of maternal and neonatal mortality and morbidity worldwide. Due to the increased prenatal surveillance and early interventions, the mortality of PE has significantly dropped in several countries, including Germany. Nevertheless, the rising burden of PE short- and long-term cardiovascular sequelae impacts both maternal and child health. Galectin-1 (gal-1), a member of the conserved family of soluble β-galactoside binding proteins, is the most abundant galectin at the maternal-fetal interface and a key regulator of the placenta-maternal dialogue due to its extracellular ability to regulate critical processes, including maternal immune and vascular adaptation to pregnancy and trophoblast differentiation and invasion properties. Dysregulation of gal-1 is associated with the development of PE in human and also PE-like syndrome in mice. Recently, we gained further insight into the maternal derived gal-1 contribution through which PE develops. Despite the increase in research on gal-1 in pregnancy, a significant knowledge gap exists regarding how intracellular gal-1 modulates cellular function (trophoblast/ maternal immune cells) by contributing to the inflammation response responsible for the unfortunate outcome in PE. We aim to study the interplay between intracellular gal-1 and the so far unknown pathways on trophoblast and maternal immune cells functions in health and PE-diseased pregnancies. Thus, our project will contribute to the understanding of the intracellular physiological role played by gal-1 adding valuable information to the management of PE disease over gestation.

• DFG Programme: Research Grants