Acta obstetricia et gynecologica Scandinavica · 2025
Adhesion molecules in the maternal-fetal interface in healthy pregnancies and preeclampsia.
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Frisch Ingrid Kverndalen, Michelsen Trond Melbye, Lekva Tove, Roland Marie Cecilie Paasche, Westerberg Ane Cecilie
Аннотация
INTRODUCTION: Adhesion molecules are markers of endothelial activation, and they are involved in placentation and inflammation. We compared levels of vascular cell adhesion molecule-1 (VCAM1), intercellular adhesion molecule-1 (ICAM1), and E-selectin (SELE) in maternal and fetal vessels of preeclampsia and healthy pregnancies. Furthermore, we investigated if the placenta releases adhesion molecules.
MATERIAL AND METHODS: Blood was sampled from three maternal (antecubital vein, uterine vein, and radial artery as a proxy for the uterine artery) and two fetal vessels (umbilical vein and artery) in 75 healthy pregnancies and 37 cases of preeclampsia undergoing cesarean delivery. Samples were also collected among 70 healthy pregnancies and 35 preeclampsia cases at three visits (gestational weeks 14-16, 22-24, and 30-32) in a longitudinal cohort. Proteins were relatively quantified on SomaLogic's 5000-multiplex platform. Venoarterial differences on both sides of the placenta were used to indicate placental release and uptake.
RESULTS: Before the onset of preeclampsia, we observed elevated maternal antecubital vein levels of VCAM1 (visits 1 and 3) and ICAM1 (all three visits). At delivery, VCAM1 and SELE were elevated in maternal vessels in preeclampsia compared to healthy, except for VCAM1 in the uterine vein. On the fetal side of the placenta, adhesion molecules were lower in preeclampsia compared to healthy pregnancies. There were no venoarterial differences on the maternal side of the placenta that indicated placental protein release. On the fetal side of the placenta, healthy controls had a positive venoarterial difference of SELE, indicating placental release to the fetus. VCAM1 and SELE levels were higher in fetal circulation as compared to maternal circulation in healthy pregnancies, whereas in preeclampsia, this was only the case for VCAM1. ICAM1 was higher in maternal than fetal circulation in healthy controls and preeclampsia.
CONCLUSIONS: Alterations in maternal levels of adhesion molecules were seen before the onset of PE. In preeclampsia, adhesion molecules were elevated in the maternal and lower in the fetal circulation. There was no placental release of the adhesion molecules to the mother, indicating a general systemic endothelial dysfunction. The results highlight new insights into the pathophysiology of preeclampsia that warrant further exploration.
MATERIAL AND METHODS: Blood was sampled from three maternal (antecubital vein, uterine vein, and radial artery as a proxy for the uterine artery) and two fetal vessels (umbilical vein and artery) in 75 healthy pregnancies and 37 cases of preeclampsia undergoing cesarean delivery. Samples were also collected among 70 healthy pregnancies and 35 preeclampsia cases at three visits (gestational weeks 14-16, 22-24, and 30-32) in a longitudinal cohort. Proteins were relatively quantified on SomaLogic's 5000-multiplex platform. Venoarterial differences on both sides of the placenta were used to indicate placental release and uptake.
RESULTS: Before the onset of preeclampsia, we observed elevated maternal antecubital vein levels of VCAM1 (visits 1 and 3) and ICAM1 (all three visits). At delivery, VCAM1 and SELE were elevated in maternal vessels in preeclampsia compared to healthy, except for VCAM1 in the uterine vein. On the fetal side of the placenta, adhesion molecules were lower in preeclampsia compared to healthy pregnancies. There were no venoarterial differences on the maternal side of the placenta that indicated placental protein release. On the fetal side of the placenta, healthy controls had a positive venoarterial difference of SELE, indicating placental release to the fetus. VCAM1 and SELE levels were higher in fetal circulation as compared to maternal circulation in healthy pregnancies, whereas in preeclampsia, this was only the case for VCAM1. ICAM1 was higher in maternal than fetal circulation in healthy controls and preeclampsia.
CONCLUSIONS: Alterations in maternal levels of adhesion molecules were seen before the onset of PE. In preeclampsia, adhesion molecules were elevated in the maternal and lower in the fetal circulation. There was no placental release of the adhesion molecules to the mother, indicating a general systemic endothelial dysfunction. The results highlight new insights into the pathophysiology of preeclampsia that warrant further exploration.