Placental endothelial nitric oxide synthase localization and expression in normal human pregnancy and pre-eclampsia

1. The aim of the present study was to investigate whether pre-eclampisa, a state of placental hypoxia, is associated with placental abnormalities in the amount, distribution and expression of enothelial nitric oxide synthase (eNOS). 2. Localization and intensity of eNOS was determined by immunohistochemistry using an antibody specific for eNOS. The amount of eNOS mRNA expression was determined by reverse transcriptionââ"šÂ¬Ã¢â‚¬Å“polymerase chain reaction (RT-PCR) and the densitometry of gel bands was expressed as a ratio of the band density of the housekeeping gene β2-microglobulin. 3. Endothelial NOS staining was localized to syncytiotrophoblast cells within the villi and decidual trophoblast cells. It was not present in the endothelium of terminal villous vessels. There was no significant difference in eNOS villous or decidual staining intensity between normal pregnancy (NP; n = 12), pre-eclampsia (n = 14), or gestational hypertension (GH; n = 4). Staining for eNOS was not significantly different in the decidua compared with the villi in NP, GH or pre-eclampsia. Within the decidua, the depth of eNOS staining was similar in NP, pre-eclampisa and GH. 4. There was no significant difference in eNOS mRNA expression between NP (0.70 ÃÆ'Ã"šÃ¢â‚¬Å¡ÃƒÆ’‚Ã"šÃ‚± 0.11), pre-eclampsia (0.5 ÃÆ'Ã"šÃ¢â‚¬Å¡ÃƒÆ’‚Ã"šÃ‚± 0.07) or GH (0.69 ÃÆ'Ã"šÃ¢â‚¬Å¡ÃƒÆ’‚Ã"šÃ‚± 0.26). 5. These findings suggest that the amount of eNOS in the placenta is not deficient in pre-eclampsia, excluding a possible pathogenic role for eNOS in this disease. Furthermore, placental hypoxia, which is associated with pre-eclampsia, did not induce an upregulation of eNOS.