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JHC exPRESS: First Published June 27, 2005. doi:10.1369/jhc.4A6480.2005
Copyright © Histochemical Society, Inc.


A more recent version of this article appeared on December 1, 2005.
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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

B. Schiessl 1, I. Mylonas 1, P. Hantschmann 1, C. Kuhn 1, S. Schulze 1, S. Kunze 1, K. Friese 1 and U. Jeschke 1*

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

* To whom correspondence should be addressed. E-mail: udo.jeschke{at}med.uni-muenchen.de.

Submitted on July 15, 2004
Accepted on 24 May 2005


   Abstract
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, nitric oxide 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{alpha}), estrogen receptor beta (ER and the endothelial NO synthase (eNOS) and inducible NO synthase (iNOS) in intra uterine 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{alpha}, ER{beta} expression. Intensity of immunohistochemical reaction was analyzed using a semi-quantitative 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 and iNOS as well as ER{beta} 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{alpha} and ER{beta} 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 intrauterine growth restriction (IUGR).

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


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