Expression of Nuclear Factor-Kappa B and Placental Apoptosis in Pregnancies Complicated with Intrauterine Growth Restriction and Preeclampsia: An Immunohistochemical Study

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  • Aban Meral
    Department of Obstetrics and Gynecology, University of Mersin
  • Cinel Leyla
    Department of Pathology, University of Mersin
  • Arslan Murat
    Department of Obstetrics and Gynecology, University of Mersin
  • Dilek Umut
    Department of Obstetrics and Gynecology, University of Mersin
  • Kaplanoglu Mustafa
    Department of Obstetrics and Gynecology, University of Mersin
  • Arpaci Rabia
    Department of Pathology, University of Mersin
  • Dilek Saffet
    Department of Obstetrics and Gynecology, University of Mersin

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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-κB) in the process is still being debated. In this work, we investigate the relationship between NF-κB expression and trophoblastic cell apoptosis in pregnancies complicated with preeclampsia or intrauterine growth restriction (IUGR) by immunohistochemical analysis of NF-κB 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-κB 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-κB and reduced bcl-2 expression.

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