Changes in endothelial cell specific molecule 1 plasma levels during preeclamptic pregnancies compared to healthy pregnancies

•From 16 until 40 weeks plasma ESM-1 is lower in control pregnant women compared to non-pregnant women.•ESM-1 plasma levels are higher during preeclampsia as compared to control pregnancies.•During preeclampsia ESM-1 levels are not different from non-pregnant women.•In both control and preeclamptic pregnancies, three months post-partum, ESM-1 plasma levels are back to non-pregnant levels. We aimed to assess the levels of endothelial cell specific molecule 1 (ESM-1) during pregnancy and preeclampsia. Plasma and placental samples were collected from women with a control pregnancy, early- or late-onset preeclamptic women and non-pregnant women (experiment 1). Plasma samples were collected between weeks 12 and birth from pregnant women at high risk for developing preeclampsia (experiment 2). ESM-1 plasma levels were measured by ELISA and in the placenta mRNA and protein were detected by immunohistochemistry and qPCR. In the first experiment we observed lower concentrations of ESM-1 in pregnant women as compared to non-pregnant women and higher concentrations during early- and late-onset preeclampsia as compared to control pregnancies of the same gestational age. Early- and late-onset preeclamptic pregnancies were not different from their subsequent controls in ESM-1 mRNA or protein levels in placental tissue. The second experiment showed that in women who had an control pregnancy, plasma ESM-1 levels were decreased as compared to non-pregnant women, from week 16 ± 2 until the end of pregnancy and returned to non-pregnant levels postpartum. In women who developed early- or late-onset preeclampsia, plasma ESM-1 was also decreased as compared to non-pregnant women from week 20 ± 2 until week 28 ± 2 of pregnancy. Then ESM-1 levels increased and were no longer different from levels in non-pregnant women on weeks 32 and 36. Plasma ESM-1 levels are decreased during pregnancy and increased in early- and late-onset preeclampsia. The source of ESM-1 is probably not the placenta, but most likely maternal endothelial cells.