Expression of estrogen receptor-alpha, estrogen receptor-beta and placental endothelial and inducible NO synthase in intrauterine growth-restricted and normal placentals.
BACKGROUND
Nitric oxide seems to play important roles in the physiology of placental blood circulation, although their expression in pathological placentas and their role is still unclear. Therefore, the aim of this study was to investigate the expression of estrogen receptor alpha (ERalpha), estrogen receptor beta (ERbeta) and the endothelial NO synthase (eNOS) and inducible NO synthase (iNOS) in intrauterine growth-restricted (IUGR) placentas, hemolysis, elevated liver enzymes, low platelets (HELLP) placentas and in normal healthy control placentas.


METHODS
Slides of paraffin-embedded placental tissue were obtained after delivery from patients diagnosed with IUGR, HELLP and normal term placentas and analyzed for eNOS and iNOS, as well as ERalpha/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.


RESULTS
Expression of eNOS and iNOS is significantly reduced in trophoblast cells of placentas with HELLP. However, ERbeta expression in HELLP placentas demonstrated a significantly elevated expression intensity compared to normal controls. ERalpha expression was not significantly different in all three pathologies investigated.


CONCLUSIONS
We speculate that the increased ERbeta expression in both syncytiotrophoblast and extravillous trophoblast cells represents accelerated proliferation of placental tissue or can be seen as a compensatory effect in HELLP placentas.
Schiessl
Barbara
B
1st Department of Obstetrics and Gynaecology, Ludwig-Maximilians-University Munich, Maistrasse, Munich, Germany.
Mylonas
Ioannis
I
Kuhn
Christina
C
Kunze
Susanne
S
Schulze
Sandra
S
Friese
Klaus
K
Jeschke
Udo
U
D047628:Estrogen Receptor alpha / Q000032:analysis* / Q000378:metabolism; D047629:Estrogen Receptor beta / Q000032:analysis* / Q000378:metabolism; D005260:Female; D005317:Fetal Growth Retardation / Q000378:metabolism*; D017359:HELLP Syndrome / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D052247:Nitric Oxide Synthase Type II / Q000032:analysis* / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000032:analysis* / Q000378:metabolism; D010920:Placenta / Q000737:chemistry* / Q000166:cytology; D011247:Pregnancy; D014327:Trophoblasts / Q000737:chemistry
D047628:Estrogen Receptor alpha; D047629:Estrogen Receptor beta; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III