Expression of nuclear factor-kappa B and placental apoptosis in pregnancies complicated with intrauterine growth restriction and preeclampsia: An immunohistochemical study


ABAN Ü. M., CİNEL Z. L., arslan m., Dilek U., KAPLANOĞLU M., Arpaci R., ...Daha Fazla

TOHOKU JOURNAL OF EXPERIMENTAL MEDICINE, cilt.204, sa.3, ss.195-202, 2004 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 204 Sayı: 3
  • Basım Tarihi: 2004
  • Doi Numarası: 10.1620/tjem.204.195
  • Dergi Adı: TOHOKU JOURNAL OF EXPERIMENTAL MEDICINE
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.195-202
  • Marmara Üniversitesi Adresli: Hayır

Özet

Preeclampsia affects 7-10% of all pregnancies, and is a major cause of maternal and fetal morbidity and mortality. Although enhanced apoptosis is well known in placentas with preeclampsia, the role of transcription factor nuclear factor-kappa B (NF-kappaB) in the process is still being debated. In this work, we investigate the relationship between NF-kappaB expression and trophoblastic cell apoptosis in pregnancies complicated with preeclampsia or intrauterine growth restriction (IUGR) by immunohistochemical analysis of NF-kappaB and three apoptosis related markers: bcl-2, caspase-3, and M30 CytoDeath antibody that identifies early apoptotic changes in the cytoskeleton related to action of caspase. The study was conducted on placental samples from 19 preeclamptic, 5 IUGR-complicated and 10 normal pregnant women. The three conclusions from the statistical analysis of the data are obtained; (i) Significantly higher expression of NF-kappaB in IUGR-complicated (p = 0.003) and preeclamptic placentas (p = 0.004) than the control placentas, (ii) significantly higher M30 index and caspase 3 expression in IUGR and preeclampsia placentas (p = 0.003), and (iii) decreased expression of bcl-2 in IUGR and preeclampsia placentas (p = 0.001). Based on these observations, we suggest that increased trophoblastic apoptosis is at least partially induced by NF-kappaB and reduced bcl-2 expression. (C) 2004 Tohoku University Medical Press.