Oxidative stress contributes to hypermethylation of Histone H3 lysine 9 in placental trophoblasts from preeclamptic pregnancies

Aberrant epigenetic regulation and increased oxidative stress in the placenta play a significant role in placental pathophysiology and fetal programming in preeclampsia, a hypertensive disorder in human pregnancy. The purpose of the study is to investigate if hypermethylation of histone H3K9 occurs...

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Bibliographic Details
Published in:Frontiers in endocrinology (Lausanne) 2024, Vol.15, p.1371220
Main Authors: Gu, Yang, Cooper, Danielle, Lewis, David F, Zoorob, Dani, Wang, Yuping
Format: Article
Language:English
Subjects:
Adult
Cells, Cultured
DNA Methylation
Female
H3K9 methylation
Histones - metabolism
Humans
hypoxia
Lysine - metabolism
Methylation
Oxidative Stress
Placenta - metabolism
placental trophoblast
Pre-Eclampsia - genetics
Pre-Eclampsia - metabolism
Pre-Eclampsia - pathology
preeclampsia
Pregnancy
superoxide dismutase
Superoxide Dismutase - genetics
Superoxide Dismutase - metabolism
Trophoblasts - metabolism
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Summary:Aberrant epigenetic regulation and increased oxidative stress in the placenta play a significant role in placental pathophysiology and fetal programming in preeclampsia, a hypertensive disorder in human pregnancy. The purpose of the study is to investigate if hypermethylation of histone H3K9 occurs in placental trophoblasts from preeclampsia. Trophoblasts were isolated and cultured from 14 placentas, 7 from normotensive pregnant women and 7 from preeclamptic pregnancies. Methylated H3K9 expression and antioxidant superoxide dismutase expression were determined by Western blot. We also examined consequences of oxidative stress and the downstream effects of histone methyltransferase inhibition on H3K9 expression associated with antioxidant CuZn-SOD and Mn-SOD expression in placental trophoblasts. We found that expression of mono-, di-, and tri-methylation of histone H3 lysine 9 (H3K9me1, H3K9me2 and H3K9me3) was significantly increased, p
ISSN:1664-2392
1664-2392
DOI:10.3389/fendo.2024.1371220