Distribution of Notch family proteins in intrauterine growth restriction and hypertension complicated human term placentas


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Şahin Z., Acar N., Ozbey O., Üstünel İ., Demir R.

ACTA HISTOCHEMICA, cilt.113, sa.3, ss.270-276, 2011 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 113 Sayı: 3
  • Basım Tarihi: 2011
  • Doi Numarası: 10.1016/j.acthis.2009.10.006
  • Dergi Adı: ACTA HISTOCHEMICA
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.270-276
  • Anahtar Kelimeler: Notch proteins, Placenta, Pregnancy-induced hypertension, Intrauterine growth restriction, Human, CELL FATE, VASCULAR DEVELOPMENT, SPIRAL ARTERIES, EXPRESSION, PREGNANCY, MOUSE, VILLI, VASCULOGENESIS, ANGIOGENESIS, RETARDATION
  • Akdeniz Üniversitesi Adresli: Evet

Özet

Members of the Notch family have been detected in many developmental and cell specification processes during placental development. However, Notch protein expression in Intrauterine Growth Restriction (IUGR) and Pregnancy Induced Hypertension (PIH) is not clear. In this study we aimed to clarify the immunolocalization of Notch proteins in full-term placentas after IUGR and PIH in comparison with normal placentas. Formalin-fixed, paraffin-embedded term placentas obtained by caesarean operations were processed for immunohistochemical localization of Notch 1, 2, 4 and Jagged 2. Transmission electron microscopy was also performed. In normal term placentas, all Notch proteins were intensely immunostained in the brush border of cells of the syncytiotrophoblast layer of the basal (maternal) side and the chorionic plate (fetal) side. The endothelial cells were also intensely immunostained in both sides for Notch 1. However, in IUGR and PIH placentas, the immunoreactivities of all Notch proteins were decreased significantly in the brush border of cells of the syncytiotrophoblast layer and the reaction was generally observed in the cytoplasm of syncytiotrophoblast cells in the basal and chorionic plate sides. The reactivity in endothelial cells was also significantly decreased. Our results have shown that the immunoreactivity and localization of Notch proteins is altered in pathologic placentas. Therefore, we propose that deregulated expression of Notch proteins may contribute to the disruption of trophoblast differentiation, endothelial cell function and/or feto-maternal traffic down-regulation during pregnancy or vice versa in such pathologic conditions.