Expression of estrogen receptor-alpha, estrogen receptor-beta and placental endothelial and inducible NO synthase in intrauterine growth-restricted and normal placentals

Arch Med Res. 2006 Nov;37(8):967-75. doi: 10.1016/j.arcmed.2006.03.011.

Abstract

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.

MeSH terms

  • Estrogen Receptor alpha / analysis*
  • Estrogen Receptor alpha / metabolism
  • Estrogen Receptor beta / analysis*
  • Estrogen Receptor beta / metabolism
  • Female
  • Fetal Growth Retardation / metabolism*
  • HELLP Syndrome / metabolism
  • Humans
  • Immunohistochemistry
  • Nitric Oxide Synthase Type II / analysis*
  • Nitric Oxide Synthase Type II / metabolism
  • Nitric Oxide Synthase Type III / analysis*
  • Nitric Oxide Synthase Type III / metabolism
  • Placenta / chemistry*
  • Placenta / cytology
  • Pregnancy
  • Trophoblasts / chemistry

Substances

  • Estrogen Receptor alpha
  • Estrogen Receptor beta
  • Nitric Oxide Synthase Type II
  • Nitric Oxide Synthase Type III