Estrogen and
progesterone are the main pregnancy
hormones produced by the placenta. It is well understood that
estrogen stimulates angiogenesis in the uterus during the reproductive cycle. Although the
estrogen and
progesterone signaling pathways are assumed to be associated with placental vascularization and
preeclampsia, expression of
estrogen receptors (ESRs) and
progesterone receptor (PGR) in the placenta have not been well studied. The present study examined the expression patterns of
steroid hormone receptors in placentas. Human placenta samples were collected and divided into normal and
preeclampsia groups. Results revealed that expression levels of ESR1 were reduced, whereas ESR2 and PGR were elevated in preeclamptic placentas. To generate an in vitro
preeclampsia environment, human placenta‑derived BeWo cells were incubated under hypoxic conditions, or treated with catechol‑O‑methyl
transferase inhibitor (COMT‑in) or L‑NG‑nitroarginine methyl
ester (L‑NAME). Expression levels of ESR1, ESR2 and PGR in hypoxic cells demonstrated similar regulation as those in placentas from women with
preeclampsia. Although COMT‑in and L‑NAME did not significantly regulate the expression levels of the receptors, COMT‑in translocated ESR2 and PGR from the nucleus to the cytoplasm, indicating that these receptors were inactivated. These results suggested that ESRs and PGR are associated with symptoms of
preeclampsia in the placenta. The expression of ESR1 was reduced in preeclamptic placenta and hypoxic BeWo cells. In addition, the activation of ESR2 and PGR was blocked in placenta cells subjected to COMT‑in treatment. The reduced ESR1 expression and inactivation of ESR2 and PGR
proteins may affect the physiological complications of
preeclampsia in the placenta.