EBF1-Correlated Long Non-coding RNA Transcript Levels in 3rd Trimester Maternal Blood and Risk of Spontaneous Preterm Birth

2020 ◽  
Author(s):  
Guoli Zhou ◽  
Claudia Holzman ◽  
Bin Chen ◽  
Ping Wang ◽  
Yujing J. Heng ◽  
...  
Keyword(s):  
Preterm Birth ◽  
Maternal Blood ◽  
Spontaneous Preterm Birth ◽  
Transcript Levels ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
Rna Transcript

Long non-coding RNA SNHG29 regulates cell senescence via p53/p21 signaling in spontaneous preterm birth

Placenta ◽  
2021 ◽  
Vol 103 ◽  
pp. 64-71
Author(s):  
Jiayi Jiang ◽  
Haoyue Hu ◽  
Qian Chen ◽  
Yi Zhang ◽  
Wenqian Chen ◽  
...  
Keyword(s):  
Preterm Birth ◽  
Cell Senescence ◽  
Spontaneous Preterm Birth ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals The Role of Epigenetics in Placental Development and the Etiology of Preeclampsia

2019 ◽  
Vol 20 (11) ◽  
pp. 2837 ◽  
Author(s):  
Clara Apicella ◽  
Camino S. M. Ruano ◽  
Céline Méhats ◽  
Francisco Miralles ◽  
Daniel Vaiman
Keyword(s):  
Maternal Blood ◽  
Placental Development ◽  
Post Translational Modifications ◽  
Epigenetic Marks ◽  
Placental Function ◽  
Non Coding Rna ◽  
The Impact ◽  
Long Non Coding Rna ◽  
Potential Use

In this review, we comprehensively present the function of epigenetic regulations in normal placental development as well as in a prominent disease of placental origin, preeclampsia (PE). We describe current progress concerning the impact of DNA methylation, non-coding RNA (with a special emphasis on long non-coding RNA (lncRNA) and microRNA (miRNA)) and more marginally histone post-translational modifications, in the processes leading to normal and abnormal placental function. We also explore the potential use of epigenetic marks circulating in the maternal blood flow as putative biomarkers able to prognosticate the onset of PE, as well as classifying it according to its severity. The correlation between epigenetic marks and impacts on gene expression is systematically evaluated for the different epigenetic marks analyzed.

A novel urinary long non-coding RNA transcript improves diagnostic accuracy in patients undergoing prostate biopsy

The Prostate ◽  
2015 ◽  
Vol 75 (6) ◽  
pp. 653-661 ◽  
Author(s):  
Wei Zhang ◽  
Shan-Cheng Ren ◽  
Xiao-Lei Shi ◽  
Ya-wei Liu ◽  
Ya-Sheng Zhu ◽  
...  
Keyword(s):  
Diagnostic Accuracy ◽  
Prostate Biopsy ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
Rna Transcript

scholarly journals Psg22 expression in mouse trophoblast giant cells is associated with gene inversion and co-expression of antisense long non-coding RNAs

Reproduction ◽  
2015 ◽  
Vol 149 (1) ◽  
pp. 125-137 ◽  
Author(s):  
John M Williams ◽  
Melanie Ball ◽  
Andrew Ward ◽  
Tom Moore
Keyword(s):  
Late Pregnancy ◽  
Giant Cells ◽  
Maternal Blood ◽  
Protein Domain ◽  
Immunoglobulin Superfamily ◽  
Genomic Locus ◽  
Non Coding Rna ◽  
Domain Organisation ◽  
Trophoblast Giant Cells ◽  
Long Non Coding Rna

Pregnancy-specific glycoproteins (PSGs) are secreted carcinoembryonic antigen (CEA)-related cell adhesion molecules-related members of the immunoglobulin superfamily and are encoded by multigene families in species with haemochorial placentation. PSGs may be the most abundant trophoblast-derived proteins in human maternal blood in late pregnancy and there is evidence that dysregulation of PSG expression is associated with gestational pathology. PSGs are produced by syncytiotrophoblast in the human placenta and by trophoblast giant cells (TGCs) and spongiotrophoblast in rodents, and are implicated in immune regulation, angiogenesis and regulation of platelet function. PSGs are encoded by 17 genes in the mouse and ten genes in the human. While functions appear to be conserved, the typical protein domain organisation differs between species. We analysed the evolution of the mouse Psg genomic locus structure and report inversion of the Psg22 gene within the locus. Psg22 is the most abundant Psg transcript detected in the first half of mouse pregnancy and we identified antisense long non-coding RNA (lncRNA) transcripts adjacent to Psg22 associated with an active local chromatin conformation. This suggests that an epigenetic regulatory mechanism may underpin high Psg22 expression relative to the other Psg gene family members in TGCs.

EBF1 Gene mRNA Levels in Maternal Blood and Spontaneous Preterm Birth

2020 ◽  
Vol 27 (1) ◽  
pp. 316-324 ◽  
Author(s):  
Guoli Zhou ◽  
Claudia Holzman ◽  
Yujing J. Heng ◽  
Mark Kibschull ◽  
Stephen J. Lye ◽  
...  
Keyword(s):  
Preterm Birth ◽  
Maternal Blood ◽  
Mrna Levels ◽  
Spontaneous Preterm Birth ◽  
Gene Mrna

Enhanced S100B expression in T and B lymphocytes in spontaneous preterm birth and preeclampsia

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Mandy Busse ◽  
Markus Scharm ◽  
Anika Oettel ◽  
Anke Redlich ◽  
Serban-Dan Costa ◽  
...  
Keyword(s):  
T Cells ◽  
Preterm Birth ◽  
B Cells ◽  
Immune Cells ◽  
Cd4 T Cells ◽  
Fetal Brain ◽  
Maternal Blood ◽  
Study Cohort ◽  
Spontaneous Preterm Birth ◽  
Elevated Liver Enzymes

Abstract Objectives S100B belongs to the family of danger signaling proteins. It is mainly expressed by glial-specific cells in the brain. However, S100B was also detected in other cell likewise immune cells. This molecule was suggested as biomarker for inflammation and fetal brain damage in spontaneous preterm birth (sPTB), preeclampsia (PE) and HELLP (hemolysis, elevated liver enzymes, and low platelet count). Methods The aim of our study was to determine the concentration of S100B in maternal and cord blood (CB) plasma and placenta supernatant as well as the expression of S100B in maternal and CB CD4+ T cells and CD19+ B cells in sPTB and patients delivering following PE/HELLP diagnosis compared to women delivering at term (TD). The S100B expression was further related to the birth weight in our study cohort. Results S100B concentration was enhanced in maternal and CB plasma of sPTB and PE/HELLP patients and positively correlated with interleukin-6 (IL-6) levels. Increased S100B was also confirmed in CB of small-for-gestational-age (SGA) infants. S100B expression in maternal blood was elevated in CD4+ T cells of PE/HELLP patients and patients who gave birth to SGA newborns as well as in CD19+ B cells of sPTB and PE/HELLP patients and patients with SGA babies. In CB, the expression of S100B was increased in CD19+ B cells of sPTB, PE/HELLP and SGA babies. Conclusions Our results support the hypothesis that S100B expression is enhanced in inflammatory events associated with preterm birth and that S100B expression in immune cells is a relevant marker for inflammation during pregnancy complications.

scholarly journals Elevated methylation of the vault RNA2-1 promoter in maternal blood is associated with preterm birth

BMC Genomics ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Young-Ah You ◽  
Eun Jin Kwon ◽  
Han-Sung Hwang ◽  
Suk-Joo Choi ◽  
Sae Kyung Choi ◽  
...  
Keyword(s):  
Preterm Birth ◽  
Large Population ◽  
Underlying Mechanism ◽  
Maternal Blood ◽  
Promoter Regions ◽  
Non Coding Rna ◽  
Genome Wide ◽  
Increased Risk ◽  
Health And Disease ◽  
Whole Blood Cells

Abstract Background Preterm birth, defined as parturition before 37 completed weeks of gestation, is associated with an increased risk of neonatal complications and death, as well as poor health and disease later in life. Epigenetics could contribute to the mechanism underlying preterm birth. Results Genome-wide DNA methylation analysis of whole blood cells from 10 women (5 term and 5 preterm deliveries) was performed using an Illumina Infinium HumanMethylation450 BeadChips array. We identified 1,581 differentially methylated CpG sites in promoter regions between term and preterm birth. Although the differences were not significant after correcting for multiple tests, seven CpGs on the genomically imprinted vault RNA2-1 (VTRNA2-1; also known as non-coding RNA, nc886 or miR-886) showed the largest differences (range: 26–39 %). Pyrosequencing verification was performed with blood samples from pregnant women recruited additionally (39 term and 43 preterm deliveries). In total, 28 (34.1 %) samples showed hypomethylation of the VTRNA2-1 promoter (< 13 % methylation), while 54 (65.9 %) samples showed elevated methylation levels between 30 and 60 %. Elevated methylation of VTRNA2-1 promoter was associated with an increased risk of preterm birth after adjusting for maternal age, season of delivery, parity and white blood cell count. The mRNA expression of VTRNA2-1 was 0.51-fold lower in women with preterm deliveries (n = 20) compared with women with term deliveries (n = 20). Conclusions VTRNA2-1 is a noncoding transcript to environmentally responsive epialleles. Our results suggest that elevated methylation of the VTRNA2-1 promoter may result in increased risk of PTB caused by the pro-inflammatory cytokines. Further studies are needed to confirm the association of VTRNA2-1 methylation with preterm birth in a large population, and to elucidate the underlying mechanism.

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