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Decreased Activation of the X‐linked inhibitor of Apoptosis Protein (XIAP) is Associated with Increased Apoptosis in the Preeclamptic Placenta
Author(s) -
Price Matthew Dean,
Arroyo Juan Alberto
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.727.10
Subject(s) - xiap , inhibitor of apoptosis , placenta , syncytiotrophoblasts , apoptosis , placentation , biology , andrology , western blot , cancer research , fetus , pregnancy , medicine , programmed cell death , gene , biochemistry , caspase , genetics
Normal placentation and placental development are critical for a successful pregnancy and mediate important steps such as implantation and delivery of nutrients to the fetus. Preeclampsia (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 active XIAP protein in PE placenta compared to controls. Control and PE placental samples were collected shortly after delivery. Tissues were frozen in liquid Nitrogen for RNA and western blot studies. For immunohistochemical studies tissues were fixed and embedded in paraffin and stained for activated (phospho) XIAP. We observed: 1) a trend for a significant decrease in XIAP gene expression (60%) in the PE placenta as compared to controls; 2) No significant differences in XIAP protein expression; 3) a significant decreased in active (phospho) XIAP protein (30%; p<0.05) in the placentas of PE women; and 4) decreased in active (phopspho) XIAP immunostaining in the syncitiotrophoblast layer of the PE placenta. Our data confirms that XIAP protein is expressed by the syncytiotrophoblasts in the human placenta during PE. We conclude that the decrease in activation of this protein during PE could potentially account for the increased apoptosis observed in this tissue at term. This result gives insights into pathways associated with the increased placental apoptosis and could be useful in the understanding of potential mechanisms that lead to placental insufficiency associated with this disease.

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