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Placental transcriptome in pregnancies complicated by Intrauterine growth restriction (IUGR) and preeclampsia (PE)

ABSTRACT: Placental transcriptome in pregnancies complicated by Intrauterine growth restriction (IUGR) and preeclampsia (PE)

PROVIDER: PRJNA472249 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7188850.fastq.gz	Fastqsanger.gz
	SRR7188860.fastq.gz	Fastqsanger.gz
	SRR7188860_1.fastq.gz	Fastqsanger.gz
	SRR7188860_2.fastq.gz	Fastqsanger.gz
	SRR7188870.fastq.gz	Fastqsanger.gz

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Placental transcriptome in pregnancies complicated by Intrauterine growth restriction (IUGR) and preeclampsia (PE)

Project description:Purpose: Identify differentially expressed genes in placental samples from early-onset (EO) IUGR, EO-PE, as well as pregnancies complicated by both EO-PE and EO-IUGR

2019-06-28 | GSE114691 | GEO

Placental microRNA expression in pregnancies complicated by Intrauterine growth restriction (IUGR) and preeclampsia (PE)

Project description:Purpose: Identify differentially expressed miRNAs in placental samples from early-onset (EO) IUGR, EO-PE, as well as pregnancies complicated by both EO-PE and EO-IUGR

2019-06-28 | GSE114349 | GEO

Placental microRNA expression in pregnancies complicated by Intrauterine growth restriction (IUGR) and preeclampsia (PE)

Project description:Placental microRNA expression in pregnancies complicated by Intrauterine growth restriction (IUGR) and preeclampsia (PE)

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Regulatory small RNA profiling of first-trimester maternal plasma-derived exosome content in preeclampsia aggravated with intrauterine growth restriction

Project description:Preeclampsia (PE) is a pregnancy related multisystemic syndrome, which shows symptomes after the 20th week of the pregnancy. It affects 5-8% of all pregnancies, caused by placental disfunction and commonly combined with fetal intrauterine growth restriction (IUGR). Exosomes mediate cell-to-cell communication with their cargo, such as different types of RNA molecules. The exosomal RNA cargo is unique, gives information about the molecular condition of the donor cells and promotes altered gene expression in the acceptor cells. To address a better understanding of the pathophysiological mechanism of PE combined with IUGR, we investigated the differences of plasma exosomal regulatory small RNA content between healthy and PE+IUGR pregnancies before the development of symptoms. We created a high-throughput exosomal small RNA sequencing based method using first-trimester maternal plasma samples from 5 control and 5 PE+IUGR pregnancies to find differences in regulatory small RNA expression levels, such as miRNAs and piRNAs. The differential exosomal expression was corrected for the completed gestational weeks at sampling time calculated on the basis of the Crown-Rump Length (CRL). The analysis has shown differential exosomal expression in case of 16 miRNAs and 6 piRNAs in the PE+IUGR pregnancies compared to normal conditions (p-value ≤ 0.05) . All of the miRNAs and 3 piRNAs were up-regulated, wherease 3 piRNAs were down-regulated. Our results also supported the importance of gestational age at sampling time on exosomal small RNA expression.

2024-02-23 | GSE241815 | GEO

Gene expression profiling indicates inflammatory pathways involved in IUGR due to placental insufficiency

Project description:Intrauterine growth restriction (IUGR) represents a major obstetric challenge with perinatal complications and a risk factor of developing disease in adult life. Placental insufficiency is one of the common features accompanying IUGR. The aim of this study was to evaluate global placental gene expression profile in IUGR compared to normal pregnancies. Placental samples were collected by eight IUGR pregnancies with placental insufficiency ascertained by Doppler and eight healthy controls. A 30K Human Genome Survey Microarray v.2.0 (Applied Biosystems) was used to evaluate global gene expression profile. Principal component analysis showed good separation in terms of gene expression patterns between the groups. Pathway analysis with Bonferroni correction for multiple testing showed significant (p<0.05) up-regulation of inflammation mediated by chemokine and cytokine signalling pathway in the IUGR placentas. Genes involved in metabolism of glucocorticoids (HSD11B1 and DHRS2) were found differentially expressed. We found no imprinted genes to be differentially expressed and only one gene involved in epigenetic modifications (MBD3) to be down-regulated in the IUGR placentas, indicating that IUGR due to placental insufficiency is not associated to placental imprinting. Subgroup analysis between pure IUGR and IUGR with preeclampsia placentas showed only 27 differentially expressed genes suggesting common pathophysiology. Eight placental samples from normal human placenta compared to eight human placental samples from patients with intrauterine growth restrictions due to placental insufficiency

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Villous trophoblast apoptosis is elevated and restricted to cytotrophoblasts in pregnancies complicated by preeclampsia, IUGR, or preeclampsia with IUGR.

Project description:Human placental villi are surfaced by an outer multinucleated syncytiotrophoblast and underlying mononucleated cytotrophoblasts. Conflicting data have attributed one, or the other, of these villous trophoblast phenotypes to undergo enhanced apoptosis in complicated pregnancies, compared to term, normotensive pregnancies. We use high-resolution confocal microscopy after co-staining for E-cadherin, as a trophoblast plasma membrane marker, and for the cleavage products of cytokeratin 18 and PARP1, as markers for caspase-mediated apoptosis, to distinguish between apoptotic cytotrophoblasts and apoptosis within the syncytiotrophoblast. We test the hypothesis that increased caspase-mediated apoptosis occurs in villi of placentas derived from pregnancies complicated by preeclampsia, intrauterine growth restriction (IUGR), or both. We find significantly elevated apoptosis in villous cytotrophoblasts from women with preeclampsia and/or IUGR, compared to term, normotensive pregnancies. Apoptosis of cytotrophoblasts in villi from complicated pregnancies appears to progress similarly to what we found previously for apoptotic cytotrophoblasts in villi from in term, normotensive pregnancies. Notably, caspase-mediated apoptosis was not detectable in regions with intact syncytiotrophoblast, suggesting strong repression of apoptosis in this trophoblast phenotype in vivo. We suggest that the elevated apoptosis in cytotrophoblasts in preeclampsia contributes to the placental dysfunction characteristic of this disorder. We also propose that repression of apoptosis in the syncytiotrophoblast is important to prevent apoptosis sweeping throughout the syncytium, which would result in widespread death of this essential interface for maternal-fetal exchange.

| S-EPMC3467099 | biostudies-literature

Altered Gene Expression Profile of Microvascular Endothelium in Placentas from IUGR/Preeclamptic Pregnancies

Project description:The placental microvasculature of the human fetus is essential for the efficient transfer of gases, nutrients and waste between the mother and fetus. Microvascular hypoplasia of the terminal villi is associated with the placental pathology observed in cases of severe Intra Uterine Growth Restriction (IUGR). We used novel methods to isolate a pure population of placental microvascular endothelial cells from control preterm placentas (n=3) and placenta complicated by severe IUGR (n=6) with superimposed preeclampsia (n=5). Distal placental villous tissue was collected to enrich for terminal villi. Tissue was minced, digested and placental microvascular endothelial cells (PlMEC) were positively selected using tocosylated magnetic Dynabeads labeled with Human Endothelial Antigen lectin. The purity of the PlMEC (95%) was assessed by CD31 immunocytochemistry. RNA was extracted from the PlMEC samples and also from 3 term placenta and subjected to Affymetrix microarray analysis (U133Plus2 array chips). Data from the 3 term placentas and 3 preterm PlMEC arrays was used to generate an endothelial cell specific gene profile. This profile was used to identify the endothelial genes differentially regulated in all 6 IUGR cases. BTNL9 and NTRK2 transcripts were upregulated and SAA1, GNAS and SLAMF1 transcripts were downregulated as relative to the preterm controls. These changes were validated by Real time PCR in the PlMEC samples. This novel study is the first to identify endothelial candidate genes that may play a role in the villous hypoplasia of severe IUGR. This work advances our understanding of the molecular defects in placental microvascular endothelial cells in normal and pathologic pregnancies.

2012-04-01 | GSE25861 | GEO

RNA-sequencing data of liver tissue of intrauterine growth restricted (IUGR) piglets with or without supplementary energy treatment

Project description:RNA-sequencing data of liver tissue of intrauterine growth restricted (IUGR) piglets with or without supplementary energy treatment

2023-03-01 | GSE226052 | GEO

Placental DNA methylation in normal and complicated pregnancies

Project description:Placental DNA methylation in normal and complicated pregnancies

| PRJNA1211636 | ENA

Gene expression profiling indicates inflammatory pathways involved in IUGR due to placental insufficiency

2008-08-01 | GSE12216 | GEO