Joost H N Schuitemaker1, Thomas I F H Cremers2, Maria G Van Pampus3, Sicco A Scherjon4, Marijke M Faas5. 1. Div. of Medical Biology, Dept. of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands; Research & Development, IQ Products BV, Groningen, The Netherlands. Electronic address: j.h.n.schuitemaker@umcg.nl. 2. Dept. Pharmaceutical Analysis, University of Groningen, Groningen, The Netherlands. 3. Onze Lieve Vrouwe Gasthuis, Dept. of Obstetrics and Gynecology, Amsterdam, The Netherlands. 4. Dept. of Obstetrics and Gynecology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands. 5. Div. of Medical Biology, Dept. of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands; Dept. of Obstetrics and Gynecology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Abstract
OBJECTIVE: We aimed to assess the levels of endothelial cell specific molecule 1 (ESM-1) during pregnancy and preeclampsia. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
OBJECTIVE: We aimed to assess the levels of endothelial cell specific molecule 1 (ESM-1) during pregnancy and preeclampsia. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.