Dynamics of Base Excision Repair at the Maternal-Fetal Interface in Pregnancies Complicated by Preeclampsia

Area of Science:

• Obstetrics and Gynecology
• Molecular Biology
• Cellular Biology

Background:

• Preeclampsia (PE) is a major global cause of maternal and perinatal mortality.
• While placental endothelial dysfunction and oxidative stress are implicated, the precise pathology of PE remains elusive.
• Previous research indicated increased DNA damage in placentas of women with PE.

Purpose of the Study:

• To investigate the role of base excision repair proteins in preeclampsia.
• To compare the expression patterns of OGG1 and APE1 in placental tissues from women with and without PE.
• To determine the cellular localization of OGG1 and APE1 under oxidative stress conditions.

Main Methods:

• An in vivo comparative study involving 20 preeclamptic and 8 healthy control subjects.
• An in vitro hypoxia/reperfusion model to simulate placental oxidative stress.
• Spatial expression analysis of 8-oxoguanine glycosylase (OGG1) and apurinic/apyrimidinic endonuclease-1 (APE1) proteins.

Main Results:

• Significantly elevated concentrations of OGG1 and APE1 were observed in PE placental tissues compared to controls (P < .0001).
• In vitro studies showed markedly higher OGG1 and APE1 expression in maternal decidual cells than in fetal cytotrophoblasts under oxidative stress (P < .0001).
• These findings highlight differential expression of DNA repair proteins in response to oxidative stress.

Conclusions:

• OGG1 and APE1 expression is upregulated in preeclamptic placentas.
• These proteins are preferentially expressed in maternal decidual cells during oxidative stress.
• OGG1 and APE1 likely play a protective role against oxidative base damage in decidual cells during preeclampsia.