286: XIAP, caspase 3 and apoptosis in the preeclamtic placenta


      Preeclampsia (PE) is a leading cause of maternal and fetal morbidity and mortality. PE is characterized by an increase in placental apoptosis, however the mechanism is not conclusive. The X-linked inhibitor of apoptosis protein (XIAP) protects against apoptosis. Our objective was to determine the level and localization of XIAP as well as the levels of caspase 3 in PE placenta compared to controls.

      Study Design

      Under IRB consent, tissue biopsies and protein lysates were made from human chorionic villi obtained from pregnancies complicated by PE (n=5) or matched controls (n=5). TUNEL Assay was performed to confirm apoptosis. XIAP localization was determined by immunohistochemistry. Western blot analyses were performed for XIAP and caspase 3. The mean±SE values for the TUNEL and western blot analyses were compared using the Wilcoxon rank sum test.


      TUNEL assay showed increased villi apoptosis in PE (p<0.007). XIAP localized to the syncytiotrophoblasts. There was a trend for decreased for XIAP protein in the PE samples (p<0.08). However, there was no significant difference for both total and activated caspase 3 between the PE and control samples.


      Our data confirms that apoptosis is increased in PE placentas. XIAP protein is expressed by the syncytiotrophoblasts in the human placenta and may be decreased in PE potentially accounting for the increased apoptosis. However, the lack of a difference in caspase 3 activation suggests that placental apoptosis in PE may occur via a caspase-independent pathway. (NIH: R01 HL071990-01A1 and an ABOG/AAOGF Award).
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