Abstract

Apoptosis within the placenta is increased in pregnancies complicated by pre-eclampsia (PE).This study aimed at evaluating the mitochondrial pathway of apoptosis in placenta of pregnant women with pre-eclampsia and correlate it with severity and pregnancy outcome . Apoptosis was assessed by measuring DNA fragmentation%,Bcl-2, p53 and caspase-9 in placental tissues from 25 pregnancies complicated by pre-eclampsia, and 25 placentas of normal pregnancy (NP). DNA fragmentation, p53 and caspase-9, were significantly increased while, Bcl-2 was significantly decreased in the placenta of pre-eclampsia group compared to control. No significant difference between mild and severe pre-eclampsia subgroupsregarding these parameters could be found. DNA fragmentation was negatively correlated with Bcl-2 in PE group. Moreover, DNA fragmentation was negatively correlated with maternal age in both PE and control groups. A significant positive correlation between placental DNA fragmentation and gestational age in the NP group was observed. A significant negative correlation between caspase-9 activity, and fetal weight in PE group was found. It can be concluded that Hypoxia and ischemia induced by pre-eclampsia, up regulate p53 and reduce Bcl-2 expression with activation of caspase-9 and increasing DNA fragmentation in placental tissue. These results implicate the mitochondrial pathway in enhancing apoptosis in preeclamptic placenta and affecting fetal outcome but not the severity.Keywords : Apoptosis, p53, Bcl-2, Caspase-9, Mitochondria,Pre-eclampsia.

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