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Expression of Endothelial NO Synthase, Inducible NO Synthase, and Estrogen Receptors Alpha and Beta in Placental Tissue of Normal, Preeclamptic, and Intrauterine Growth-restricted Pregnancies

Barbara Schiessl, Ioannis Mylonas, Peer Hantschmann, Christina Kuhn, Sandra Schulze, Susi Kunze, Klaus Friese and Udo Jeschke

Ludwig-Maximilians-University Munich, 1st Department of Obstetrics and Gynaecology, Maistrasse 11, 80337 Munich, Germany

Correspondence to: PD Dr. rer. nat. Udo Jeschke, Ludwig-Maximilians-University Munich, 1st Department of Obstetrics and Gynaecology, Maistrasse 11, 80337 Munich, Germany. E-mail: udo.jeschke{at}med.uni-muenchen.de

In the physiology of placental blood circulation, nitric oxide (NO) synthases seem to play important roles, although their expression in pathological placentas and their role is still unclear. In addition, NO synthase activation seems to be related to estrogen receptor expression. Therefore, the aims of this study were to investigate the expression of estrogen receptors alpha (ER), estrogen receptor beta (ER and the endothelial NO synthase (eNOS), and inducible NO synthase (iNOS) in intrauterine growth-restricted (IUGR) placentas, preeclamptic placentas, and in normal healthy control placentas. Slides of paraffin-embedded placental tissue were obtained after delivery from patients diagnosed with IUGR, preeclampsia, and normal term placentas and analyzed for eNOS, iNOS as well as ER and ERß expression. Intensity of immunohistochemical reaction was analyzed using a semiquantitative score and statistical analysis was performed. In addition, Western blot experiments were performed for comparison of staining intensities obtained by immunohistochemistry and western blot. Expression of eNOS, iNOS, and ERß is significantly reduced in trophoblast cells of placentas with IUGR. However, preeclamptic placentas demonstrated a significant elevated expression intensity of these proteins compared with normal controls. A different expression of eNOS, iNOS, ER, and ERß by human trophoblast cells seems to results in lower NO output and impaired trophoblast invasion. Results obtained in our study provide evidence that reduced expression of the investigated proteins is related to IUGR. (J Histochem Cytochem 53:1441–1449, 2005)

Key Words: nitric oxide synthases • estrogen receptor alpha/beta • intrauterine growth restriction • preeclampsia

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