Vol 80, No 9 (2009)
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Expression of caspase-3, Bax nad Bcl-2 in placentas from pregnancies complicated by treated and non-treated fetal growth restriction

Agnieszka nawrocka-Kunecka, Urszula Kowalska-Koprek, Anita Szczerba, Agata Karowicz-Bilińska, Grzegorz Bartosz
Ginekol Pol 2009;80(9).

Abstract

Abstract Background: Fetal growth restriction (FGR) is the reason of high prematurity rate and its later complications. Restriction of utero-placental circulation, which could be changed by IURG treatment, plays the main role in FGR. The results of changes in apoptosis-related genes expression due to FGR treatment may help further in the prevention and treatment of FGR. Material and methods: Caspase-3, Bax and Bcl-2 expressions in normal pregnancies and those complicated by treated and untreated FGR have been compared. The study was conducted in 2005-2006 at the High-Risk Pregnancy Unit of Medical University in Łódź and Kopernik Hospital in Łódź. Caspase-3, Bax and Bcl-2 expressions were assessed by immunohistochemical method. Bcl-2 was assessed in the trophoblast, Bax and caspase-3 in the decidua and the trophoblast. Results: The mean value of Bcl-2 in the trophoblast was 58.8±12.7 in the FGR-untreated group, 37.0±0.5 in the FGR-treated group and 65.7±6.9 in the control group. In the FGR-untreated group the mean value of Bax expression was 60.6±10.7 in the trophoblast and 32.0±7.3 in the decidua. In the FGR-treated group the mean value of Bax expression was 42.2±12.2 in the trophoblast and 20.9±6.4 in the decidua. In the control group the mean value of Bax expression was 13.6±2.2 in the trophoblast and 6.6±6.8 in the decidua. In the FGR-untreated group the mean value of Cpp-32 expression was 40.1±9.1 in the trophoblast and 42.6±.12.5 in the decidua. In the FGR-treated group the mean value of Cpp-32 expression was 21.3±6.8 in the trophoblast and 23.7±5.1 in the decidua. In the control group the mean value of Cpp-32 expression was 13,6±6,3 in trophoblast and 11.6±5.3 in the decidua. Conclusions: Increased expression of pro-apoptotic proteins in the placenta might be one of the reasons for FGR development. The treatment used in the FGR group decreased the process of apoptosis.

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