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Apoptotic signaling is augmented in the preeclamptic placenta (796.9)
Author(s) -
Horvat Darijana,
Leonard Dean,
Allen Steven,
Jones Richard,
Beeram Madhava,
Kuehl Thomas,
Uddin Mohammad
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.796.9
Subject(s) - placenta , umbilical cord , western blot , apoptosis , preeclampsia , andrology , oxidative stress , medicine , signal transduction , p38 mitogen activated protein kinases , fetus , biology , endocrinology , mapk/erk pathway , pregnancy , immunology , microbiology and biotechnology , biochemistry , genetics , gene
Objective: Preeclampsia (preE), a syndrome of hypertension and proteinuria in pregnancy, is thought to be initiated with alterations of placental function. Hypoxia and oxidative stress can lead to placental apoptosis. We assessed apoptotic signaling in tissues from patients and rats with or without preE. Methods: Samples of placenta and umbilical cord were collected from 10 normal pregnant (NP) and 10 preE consenting patients in an IRB approved prospective study. Ten rats with preE and 10 NP rats also were used. Apoptotic and stress signaling protein (Bax, Bcl 2 , Cox‐2) expression and p38 MAPK phosphorylation were assayed by western blot and immunohistochemistry. Comparisons were performed using ANOVA with Duncan’s post‐hoc test. Results: Expression of Bax (Placenta: 1.2 fold, Cord: 1.5 fold), Bcl 2 (Placenta: 1.7 fold, Cord: 1.7 fold), Cox‐2 (Placenta: 0.8 fold, Cord: 2.5 fold) and p38 MAPK phosphorylation (Placenta: 1.5 fold, Cord: 1.7 fold) were up‐regulated (p<0.05) in placental tissues and umbilical cords of preE compared to NP patients. Apoptotic signaling was upregulated in preE rat placentas (Bax: 1.4 fold, Bcl 2 : 2.3 fold, Cox‐2: 2.5 fold, p38: 3.0 fold) compared to controls. Conclusions: Apoptotic signaling is augmented in preE which may lead to reduced nutrient transport capacity triggering placenta release of vascular factors that produce maternal vascular responses characteristic of this syndrome. Grant Funding Source : N/A