Immunohistochemical Evaluation of Pecam-1 (CD-31) and Icam-3 (CD-50) in Preeclamptic Placenta


Lortlar N., Kilic S., Bardakci Y., Budak G., ÖMEROĞLU S.

TURKIYE KLINIKLERI TIP BILIMLERI DERGISI, cilt.29, sa.5, ss.1131-1136, 2009 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 29 Sayı: 5
  • Basım Tarihi: 2009
  • Dergi Adı: TURKIYE KLINIKLERI TIP BILIMLERI DERGISI
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.1131-1136
  • Gazi Üniversitesi Adresli: Evet

Özet

Objective: Preeclampsia has been related to abnormalities in cellular adhesion molecule expression. Preeclampsia complicates 3-5% of all pregnancies in the world. Our primary objective was to compare the expression of two intercellular adhesion molecules, platelet endothelial cell adhesion molecule (PECAM-1/CD-31) and intercellular adhesion molecule-3 (ICAM-3/CD-50) in preeclamptic and healthy placental beds. Material and Methods: A prospective controlled clinical trial was conducted involving placentas from 30 women with preeclampsia and 30 normal pregnant women. Formalin Fixed and paraffin embedded placental sections were analyzed using peroxidase-antiperoxidase indirect immunohistochemical methods. Two different investigators evaluated the intensity of staining independently. The intensity of the immunreactivity was analyzed using a semi-quantitative score and statistical analyses were performed, during which Kolmogorov-Smirnov, Student's t, and Mann-Whitney U tests were applied to clinical and histopathological data. Results: PECAM-1 immunoreactivity was high in placental trophoblasts of preeclamptic women and in their vessel endothelium when compared with the normal placenta. On the other hand, no significant differences were found in ICAM-3 intensity between pre-eclampsia and control group placentas. Conclusions: Increased immunoreactivity of PECAM-1 in endothelial cells may cause endothelial injury, but it seems that ICAM-3 (CD-50) may be irrelevant to the etiopathogenesis of preeclampsia.