Upregulation of histone H3K9 methylation in fetal endothelial cells from preeclamptic pregnancies.

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Abstrakt

Tytuł:: Upregulation of histone H3K9 methylation in fetal endothelial cells from preeclamptic pregnancies.
Autorzy:: Sheng W; Department of Obstetrics and Gynecology, Louisiana State University Health Sciences Center-Shreveport, Shreveport, Louisiana.; Department of Obstetrics and Gynecology, First Affiliated Hospital, Harbin Medical University, Harbin, China.
Gu Y; Department of Obstetrics and Gynecology, Louisiana State University Health Sciences Center-Shreveport, Shreveport, Louisiana.
Chu X; Department of Obstetrics and Gynecology, Louisiana State University Health Sciences Center-Shreveport, Shreveport, Louisiana.; Department of Obstetrics and Gynecology, Second Affiliated Hospital, Harbin Medical University, Harbin, China.
Morgan JA; Department of Obstetrics and Gynecology, Louisiana State University Health Sciences Center-Shreveport, Shreveport, Louisiana.
Cooper DB; Department of Obstetrics and Gynecology, Louisiana State University Health Sciences Center-Shreveport, Shreveport, Louisiana.
Lewis DF; Department of Obstetrics and Gynecology, Louisiana State University Health Sciences Center-Shreveport, Shreveport, Louisiana.
McCathran CE; Department of Obstetrics and Gynecology, Louisiana State University Health Sciences Center-Shreveport, Shreveport, Louisiana.
Wang Y; Department of Obstetrics and Gynecology, Louisiana State University Health Sciences Center-Shreveport, Shreveport, Louisiana.
Źródło:: Journal of cellular physiology [J Cell Physiol] 2021 Mar; Vol. 236 (3), pp. 1866-1874. Date of Electronic Publication: 2020 Jul 23.
Typ publikacji:: Journal Article
Język:: English
Imprint Name(s):: Publication: New York, NY : Wiley-Liss
Original Publication: Philadelphia, Wistar Institute of Anatomy and Biology.
MeSH Terms:: Up-Regulation*
Endothelial Cells/*metabolism
Endothelial Cells/*pathology
Fetus/*pathology
Histones/*metabolism
Lysine/*metabolism
Pre-Eclampsia/*metabolism
Adult ; Cell Hypoxia ; Down-Regulation ; Female ; Histocompatibility Antigens/metabolism ; Histone-Lysine N-Methyltransferase/metabolism ; Human Umbilical Vein Endothelial Cells/metabolism ; Humans ; Methylation ; Nitric Oxide Synthase Type III/metabolism ; Oxidative Stress ; Placenta/metabolism ; Pregnancy ; Superoxide Dismutase/metabolism
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Contributed Indexing:: Keywords: CuZn-SOD; H3K9 methylation; endothelial cells; fetal programming; oxidative stress; preeclampsia
Substance Nomenclature:: 0 (Histocompatibility Antigens)
0 (Histones)
EC 1.14.13.39 (Nitric Oxide Synthase Type III)
EC 1.15.1.1 (Superoxide Dismutase)
EC 2.1.1.43 (EHMT2 protein, human)
EC 2.1.1.43 (Histone-Lysine N-Methyltransferase)
K3Z4F929H6 (Lysine)
Entry Date(s):: Date Created: 20200724 Date Completed: 20210914 Latest Revision: 20210914
Update Code:: 20240104
DOI:: 10.1002/jcp.29970
PMID:: 32700783
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Adverse intrauterine environment has been considered a predisposing factor for fetal programming in preeclampsia. Using human umbilical vein endothelial cells (HUVECs), we specifically explored if aberrant histone methylation occurs in fetal endothelial cells in preeclampsia. Strikingly, we found that increased di-, and tri-methylation of histone H3 lysine 9 (H3K9me2 and H3K9me3) expression were associated with upregulation of methyltransferase G9a and downregulation of endothelial nitric oxide synthase and CuZn-SOD expression in preeclamptic HUVECs. We further demonstrated that hypoxia-induced hypermethylation of H3K9 and reduced CuZn-SOD expression mimicked what were seen in preeclamptic HUVECs and inhibition of G9a could attenuate these hypoxia-induced adverse events. Our study was the first to identify hypermethylation status in fetal endothelial cells in preeclampsia, which provides plausible evidence that increased oxidative stress in the intrauterine environment is likely a mechanism to induce aberrant histone modification in fetal endothelial cells which may have a significant impact on fetal programming in preeclampsia.
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