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

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...

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Veröffentlicht in:The Tohoku Journal of Experimental Medicine 2004, Vol.204(3), pp.195-202
Hauptverfasser: Aban, Meral, Cinel, Leyla, Arslan, Murat, Dilek, Umut, Kaplanoglu, Mustafa, Arpaci, Rabia, Dilek, Saffet
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Sprache:eng
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Zusammenfassung: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.
ISSN:0040-8727
1349-3329
DOI:10.1620/tjem.204.195