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Increased X‐linked inhibitor of apoptosis‐associated factor 1 and decreased activation of the X‐linked inhibitor of apoptosis protein are associated with increased apoptosis in the preeclamptic placenta at term (541.11)
Author(s) -
Mejia Camilo,
Arroyo Juan,
Price Matthew
Publication year - 2014
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.28.1_supplement.541.11
Subject(s) - xiap , inhibitor of apoptosis , apoptosis , placenta , preeclampsia , western blot , biology , chemistry , cancer research , andrology , programmed cell death , medicine , fetus , pregnancy , gene , biochemistry , caspase , genetics
Preeclampsia (PE) is associated with placental insufficiencies and is characterized by an increase in placental apoptosis. Several mechanisms had been suggested but not much information is available on the role of the inhibitor of apoptosis family (IAP) of proteins. The X‐linked inhibitor of apoptosis protein (XIAP) is one of the most potent members of the IAP family of proteins. Its activation is controlled by the X‐linked of apoptosis associated factor 1 (XAF1). Our objective was to determine the level of XAF1 and its correlation with 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 western blot studies. We observed: 1) No significant differences in XIAP protein expression; 2) a significant decrease in active (phospho) XIAP protein (30%; p<0.05) in the placentas of PE women; and 4) a significant increase (38%; p<0.008) for XAF1 during preeclampsia. We conclude that the decrease in XAIP activation during PE could potentially account for the increased apoptosis observed in this tissue at term. Also, that a mechanism for this decreased XIAP activation involves increasing placental XAF1 during preeclampsia. 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.