scholarly journals Comparative gene expression profiling of placentas from patients with severe pre-eclampsia and unexplained fetal growth restriction

2011 ◽  
Vol 9 (1) ◽  
pp. 107 ◽  
Author(s):  
Haruki Nishizawa ◽  
Sayuri Ota ◽  
Machiko Suzuki ◽  
Takema Kato ◽  
Takao Sekiya ◽  
...  
2016 ◽  
Vol 46 (14) ◽  
pp. 2999-3011 ◽  
Author(s):  
A. B. Janssen ◽  
L. E. Capron ◽  
K. O'Donnell ◽  
S. J. Tunster ◽  
P. G. Ramchandani ◽  
...  

BackgroundMaternal prenatal stress during pregnancy is associated with fetal growth restriction and adverse neurodevelopmental outcomes, which may be mediated by impaired placental function. Imprinted genes control fetal growth, placental development, adult behaviour (including maternal behaviour) and placental lactogen production. This study examined whether maternal prenatal depression was associated with aberrant placental expression of the imprinted genes paternally expressed gene 3 (PEG3), paternally expressed gene 10 (PEG10), pleckstrin homology-like domain family a member 2 (PHLDA2) and cyclin-dependent kinase inhibitor 1C (CDKN1C), and resulting impaired placental human placental lactogen (hPL) expression.MethodA diagnosis of depression during pregnancy was recorded from Manchester cohort participants’ medical notes (n = 75). Queen Charlotte's (n = 40) and My Baby and Me study (MBAM) (n = 81) cohort participants completed the Edinburgh Postnatal Depression Scale self-rating psychometric questionnaire. Villous trophoblast tissue samples were analysed for gene expression.ResultsIn a pilot study, diagnosed depression during pregnancy was associated with a significant reduction in placental PEG3 expression (41%, p = 0.02). In two further independent cohorts, the Queen Charlotte's and MBAM cohorts, placental PEG3 expression was also inversely associated with maternal depression scores, an association that was significant in male but not female placentas. Finally, hPL expression was significantly decreased in women with clinically diagnosed depression (44%, p < 0.05) and in those with high depression scores (31% and 21%, respectively).ConclusionsThis study provides the first evidence that maternal prenatal depression is associated with changes in the placental expression of PEG3, co-incident with decreased expression of hPL. This aberrant placental gene expression could provide a possible mechanistic explanation for the co-occurrence of maternal depression, fetal growth restriction, impaired maternal behaviour and poorer offspring outcomes.


Cell Cycle ◽  
2018 ◽  
Vol 17 (2) ◽  
pp. 182-190 ◽  
Author(s):  
Thy P. H. Nguyen ◽  
Hannah E. J. Yong ◽  
Tejasvy Chollangi ◽  
Shaun P. Brennecke ◽  
Susan J. Fisher ◽  
...  

2014 ◽  
Vol 56 (4) ◽  
pp. 559-565 ◽  
Author(s):  
Taketoshi Yoshida ◽  
Ichiro Takasaki ◽  
Hirokazu Kanegane ◽  
Satomi Inomata ◽  
Yasunori Ito ◽  
...  

Genes ◽  
2020 ◽  
Vol 11 (10) ◽  
pp. 1146
Author(s):  
Maya A. Deyssenroth ◽  
Qian Li ◽  
Carlos Escudero ◽  
Leslie Myatt ◽  
Jia Chen ◽  
...  

Preeclampsia is a multi-systemic syndrome that presents in approximately 5% of pregnancies worldwide and is associated with a range of subsequent postpartum and postnatal outcomes, including fetal growth restriction. As the placenta plays a critical role in the development of preeclampsia, surveying genomic features of the placenta, including expression of imprinted genes, may reveal molecular markers that can further refine subtypes to aid targeted disease management. In this study, we conducted a comprehensive survey of placental imprinted gene expression across early and late onset preeclampsia cases and preterm and term normotensive controls. Placentas were collected at delivery from women recruited at the Magee-Womens Hospital prenatal clinics, and expression levels were profiled across 109 imprinted genes. We observed downregulation of placental Mesoderm-specific transcript (MEST) and Necdin (NDN) gene expression levels (false discovery rate (FDR) < 0.05) among early onset preeclampsia cases compared to preterm controls. No differences in placental imprinted gene expression were observed between late onset preeclampsia cases and term controls. While few studies have linked NDN to pregnancy complications, reductions in MEST expression levels, as observed in our study, are consistently reported in the literature in relation to various pregnancy complications, including fetal growth restriction, suggesting a potential role for placental MEST expression as a biosensor of an adverse in utero environment.


2021 ◽  
Vol 11 ◽  
Author(s):  
Xue Wang ◽  
Hong Zhu ◽  
Lei Lei ◽  
Yang Zhang ◽  
Chao Tang ◽  
...  

Fetal growth restriction (FGR) is a common pregnancy complication and a risk factor for infant death. Most patients with FGR have preeclampsia, gestational diabetes mellitus, or other etiologies, making it difficult to determine the specific molecular mechanisms underlying FGR. In this study, an integrated analysis was performed using gene expression profiles obtained from Gene Expression Omnibus. Differentially expressed genes (DEGs) between healthy and FGR groups were screened and evaluated by functional enrichment and network analyses. In total, 80 common DEGs (FDR &lt; 0.05) and 17 significant DEGs (FDR &lt; 0.005) were screened. These genes were enriched for functions in immune system dysregulation in the placenta based on Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses. Among hub genes identified as candidates for FGR and fetal reprogramming, LEP, GBP5, HLA–DQA1, and CTGF were checked by quantitative polymerase chain reaction, immunohistochemistry, and western blot assays in placental tissues. Immune imbalance could cause hypoxia environment in placenta tissues, thus regulating the fetal-reprogramming. A significant association between CTGF and HIF-1α levels was confirmed in placenta tissues and HTR8 cells under hypoxia. Our results suggest that an immune imbalance in the placenta causes FGR without other complications. We provide the first evidence for roles of CTGF in FGR and show that CTGF may function via HIF-1α-related pathways. Our findings elucidate the pathogenesis of FGR and provide new therapeutic targets.


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