Matrix Metalloproteinase 1 in Pre-eclampsia and Fetal Growth Restriction: Reduced Gene Expression in Decidual Tissue and Protein Expression in Extravillous Trophoblasts

Placenta ◽  
2010 ◽  
Vol 31 (7) ◽  
pp. 615-620 ◽  
Author(s):  
I.A. Lian ◽  
J.H. Toft ◽  
G.D. Olsen ◽  
M. Langaas ◽  
L. Bjørge ◽  
...  
Keyword(s):  
Gene Expression ◽  
Matrix Metalloproteinase ◽  
Protein Expression ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Growth Restriction ◽  
Decidual Tissue ◽  
Matrix Metalloproteinase 1 ◽  
Extravillous Trophoblasts

Membrane-Type Matrix Metalloproteinase 1 Regulates Trophoblast Functions and Is Reduced in Fetal Growth Restriction

2013 ◽  
Vol 182 (5) ◽  
pp. 1563-1571 ◽  
Author(s):  
Ursula Hiden ◽  
Nassim Ghaffari-Tabrizi ◽  
Martin Gauster ◽  
Carmen Tam-Amersdorfer ◽  
Irene Cetin ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Growth Restriction ◽  
Matrix Metalloproteinase 1 ◽  
Membrane Type

scholarly journals Maternal prenatal depression is associated with decreased placental expression of the imprinted gene PEG3

2016 ◽  
Vol 46 (14) ◽  
pp. 2999-3011 ◽  
Author(s):  
A. B. Janssen ◽  
L. E. Capron ◽  
K. O'Donnell ◽  
S. J. Tunster ◽  
P. G. Ramchandani ◽  
...  
Keyword(s):  
Gene Expression ◽  
Maternal Depression ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Growth Restriction ◽  
Prenatal Depression ◽  
Placental Lactogen ◽  
Maternal Behaviour ◽  
Imprinted Genes ◽  
Neurodevelopmental Outcomes

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.

Utility of Diagnosing Various Histological Patterns of Diffuse Chronic Hypoxic Placental Injury

2012 ◽  
Vol 15 (1) ◽  
pp. 13-23 ◽  
Author(s):  
Jerzy Stanek
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Significant Proportion ◽  
Giant Cells ◽  
Growth Restriction ◽  
Cesarean Sections ◽  
Hypertensive Disorders ◽  
Laminar Necrosis ◽  
Meconium Staining ◽  
Extravillous Trophoblasts

To examine the clinicopathologic correlations of three histological patterns of diffuse chronic hypoxic placental injury (preuterine [PR], uterine [UH], and postuterine [PU]), a retrospective statistical analysis of a large 14-year placental database was performed. Of 5097 placentas between 20 and 43 weeks of gestation examined consecutively, 4413 did not feature histological chronic placental hypoxia, while 684 did. In the latter, maternal hypertensive disorders, diabetes mellitus, abnormal cardiotocography and Dopplers, cesarean sections, inductions of labor, and fetal growth restriction, as well as other placental hypoxic lesions and decidual arteriolopathy, were statistically significantly more common than in the remaining placental material. Two hundred eighty-nine PR cases featured the most advanced gestational age and meconium staining; 237 UH cases featured severe preeclampsia, decidual arteriolopathy, villous infarction, membrane laminar necrosis, microscopic chorionic pseudocysts, excessive extravillous trophoblasts, and maternal floor multinucleate trophoblastic giant cells; and 158 PU cases featured the lowest placental weight and the highest prevalence of abnormal Dopplers, umbilical cord compromise, fetal growth restriction, cesarean section rate, and complicated 3rd stage of labor. The specificity of chronic hypoxic patterns of placental injury was much higher than the sensitivity, with the highest specificity for an excessive amount of extravillous trophoblasts. Diagnosing various hypoxic patterns of placental injury by histology may help to clarify the etiopathogenesis of a significant proportion of complications of pregnancy and abnormal fetal or neonatal outcomes. The patterns should help to retrospectively diagnose placental hypoxia, even in clinically unsuspected cases.

scholarly journals Altered downstream target gene expression of the placental Vitamin D receptor in human idiopathic fetal growth restriction

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 ◽  
...  
Keyword(s):  
Gene Expression ◽  
Vitamin D ◽  
Vitamin D Receptor ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Target Gene ◽  
Growth Restriction ◽  
Target Gene Expression ◽  
Downstream Target ◽  
Downstream Target Gene

scholarly journals Differences in Placental Imprinted Gene Expression across Preeclamptic and Non-Preeclamptic Pregnancies

Genes ◽  
2020 ◽  
Vol 11 (10) ◽  
pp. 1146
Author(s):  
Maya A. Deyssenroth ◽  
Qian Li ◽  
Carlos Escudero ◽  
Leslie Myatt ◽  
Jia Chen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Fetal Growth ◽  
Pregnancy Complications ◽  
Fetal Growth Restriction ◽  
Late Onset ◽  
Critical Role ◽  
Growth Restriction ◽  
Imprinted Genes ◽  
Imprinted Gene ◽  
Expression Levels

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.

scholarly journals Integrated Analysis of Key Genes and Pathways Involved in Fetal Growth Restriction and Their Associations With the Dysregulation of the Maternal Immune System

2021 ◽  
Vol 11 ◽  
Author(s):  
Xue Wang ◽  
Hong Zhu ◽  
Lei Lei ◽  
Yang Zhang ◽  
Chao Tang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Immune System ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Growth Restriction ◽  
Functional Enrichment ◽  
Integrated Analysis ◽  
Network Analyses ◽  
Fetal Reprogramming ◽  
Immune Imbalance

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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