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Apoptotic and stress signaling markers are augmented in preeclamptic placenta and umbilical cord
Syeda H Afroze1, Ram R Kalagiri2, Michelle Reyes3
1Department of Medical Physiology, Texas A&M Health Science Center College of Medicine, Temple, TX, USA.
Insights
Preeclampsia elevates apoptotic and stress signaling in placental and umbilical cord tissues, potentially impacting fetal development. These changes may explain complications observed in newborns born to mothers with preeclampsia.
Area of Science:
- Obstetrics and Gynecology
- Perinatal Medicine
- Molecular Biology
Background:
- Preeclampsia (preE) is linked to placental dysfunction, leading to stress and apoptotic signaling that affects fetal circulation.
- These placental changes can result in persistent defects in the offspring's circulatory system.
Purpose of the Study:
- To assess and compare apoptotic signaling pathways in placental and umbilical cord tissues from normal pregnant (NP) women and those with preeclampsia.
- To investigate the expression of key proteins involved in apoptosis and inflammation.
Main Methods:
- Prospective study involving placental and cord tissues from 27 NP and 20 preE patients.
- Western blot and immunohistochemistry used to evaluate p38 mitogen-activated protein kinase (MAPK) phosphorylation, Bax, Bcl-2, caspase-9, and cyclooxygenase-2 (Cox-2).
- Statistical comparisons performed using Student's t-test.
Main Results:
- Significantly increased p38 MAPK phosphorylation, Bax/Bcl-2 ratio, caspase-9, and Cox-2 levels were observed in preeclampsia tissues (placenta and cord) compared to normal controls (p < 0.05).
- Infants born to mothers with preeclampsia experienced longer hospital stays and multiple complications, unlike the normal pregnancy group.
Conclusions:
- Apoptotic and stress signaling pathways are heightened in preeclampsia placenta and cord tissues.
- These augmented signaling pathways contribute to an altered intrauterine environment.
- Detrimental signaling is transported to the fetus, potentially causing adverse outcomes.
Objective:
Preeclampsia (preE) has a significant link to alterations of placental function leading to stress and apoptotic signaling, which pass the placental barrier and leave persistent defect in the circulation of the offspring. We assessed apoptotic signaling in placentas and umbilical cords from patients with and without preE.
Methods:
We collected placental and cord tissues from 27 normal pregnant (NP) women and 20 preE consenting patients after delivery in an IRB approved prospective study. p38 mitogen-activated protein kinase (p38 MAPK) phosphorylation, pro-apoptotic Bcl-2-associated X (Bax), anti-apoptotic Bcl-2, caspase-9, and pro-inflammatory cyclooxygenase-2 (Cox-2) were evaluated by western blot and immunohistochemistry. Comparisons were performed using Student's t-test.
Results:
p38 phosphorylation (Placenta: 1.5 fold, Cord: 1.7 fold), ratio of Bax/Bcl-2 (Placenta: 1.7 fold, Cord: 2.2 fold), caspase-9 (Placenta: 1.5 fold, Cord: 1.8 fold) and Cox-2 (Placenta: 2.5 fold, Cord: 2.3 fold) were up-regulated (p < 0.05) in preE compared to NP patients. Average hospital stays for preE babies were longer than NP babies. No complications were reported for NP babies; however, all of preE babies had multiple complications.
Conclusions:
Apoptotic and stress signaling are augmented in preE placenta and cord tissue that alter the intrauterine environment and activates the detrimental signaling that is transported to fetus.
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