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Reduced placental expression of Regulator of G Protein Signaling-2 during preeclampsia

ABSTRACT: Reduced placental expression of Regulator of G Protein Signaling-2 during preeclampsia

PROVIDER: PRJNA505433 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8187050_1.fastq.gz	Fastqsanger.gz
	SRR8187050_2.fastq.gz	Fastqsanger.gz
	SRR8187051_1.fastq.gz	Fastqsanger.gz
	SRR8187051_2.fastq.gz	Fastqsanger.gz
	SRR8187052_1.fastq.gz	Fastqsanger.gz

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Reduced placental expression of Regulator of G Protein Signaling-2 during preeclampsia

Project description:This experiment examined effects of reduced placental Regulator of G protein Signaling-2 (Rgs2) upon the placental transcriptome in C57BL/6J mice at gestational day 12.5.

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Placental Immune alterations in early-onset preeclampsia and late-onset preeclampsia

Project description:Preeclampsia is a severe placenta-related pregnancy disorder that is generally divided into two subtypes named early-onset preeclampsia (onset <34 weeks of gestation), and lateonset preeclampsia (onset ≥34 weeks of gestation), with distinct pathophysiological origins. Both forms of preeclampsia have been associated with maternal systemic inflammation. However, alterations in the placental immune system have been less well characterized. Here, we studied immunological alterations in early- and late-onset preeclampsia placentas using a targeted expression profile approach. RNA was extracted from snap-frozen placenta samples (healthy n=13, early-onset preeclampsia n=13, and late-onset preeclampsia n=6). The expression of 730 immune-related genes from the Pan Cancer Immune Profiling Panel was measured, and the data were analyzed Q10 in the advanced analysis module of nSolver software (NanoString Technology). The results showed that early-onset preeclampsia placentas displayed reduced expression of complement, and toll-like receptor (TLR) associated genes, specifically TLR1 and TLR4. Mast cells and M2 macrophages were also decreased in early-onset preeclampsia compared to healthy pl acentas. The findings were confirmed by an immunohistochemistry approach using 20 healthy, 19 early-onset preeclampsia, and 10 late-onset preeclampsia placentas. We conclude that the placental innate immune system is altered in early-onset preeclampsia compared to uncomplicated pregnancies. The absence of these alterations in late-onset preeclampsia placentas indicates dissimilar immunological profiles. The study revealed distinct pathophysiological processes in earlyonset and late-onset preeclampsia placentas and imply that a tailored treatment to each subtype is desirable.

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Genome-wide analysis of placental gene expression in severe preterm preeclampsia

Project description:Analysis of genome-wide gene expression in placentas from women with preterm severe preeclampsia, with or without HELLP syndrome, compared to gestational age-matched controls. The hypothesis tested in the present study was that placental transcriptomic changes in preeclampsia are considerably different from controls. The results provide important information on placental transcriptomic changes in preeclampsia.

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GLOBAL ANALYSIS OF CIRCULATING AND PLACENTAL MICRORNA SIGNATURES AND PREECLAMPSIA DEVELOPMENT

Project description:We perform placental microRNA expression profiling to identify potential microRNAs involved in the development and pathogenesis of preeclampsia. microRNA expression profiling for serum was quantified by qPCR and evaluated at 12, 16, and 20 gestational weeks and at the time of preeclampsia diagnosis. Two groups were evaluated using TaqMan Low Density Array plates: a control group with 18 normotensive pregnant women and a preeclampsia group with 16 patients who developed preeclampsia during the follow-up period. The placental microRNA profile was assayed at delivery (7 cases and 7 controls) using the Illumina GAIIx sequencing platform.

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Project description:The placenta mediates adverse pregnancy outcomes, including preeclampsia, characterized by gestational hypertension and proteinuria. Placental cell type heterogeneity in preeclampsia is not well-understood and limits mechanistic interpretation of bulk gene expression measures. We generated single-cell RNA-sequencing samples for integration with existing data to create the largest deconvolution reference of 19 fetal and 8 maternal cell types from placental villous tissue at term. We deconvoluted eight published microarray case-control studies of preeclampsia. Our findings indicate substantial placental cellular heterogeneity in preeclampsia that predict previously observed bulk gene expression differences. Our deconvolution reference lays the groundwork for cellular heterogeneity-aware investigation into placental dysfunction and adverse birth outcomes.

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Placental Immune alterations in early-onset preeclampsia and late-onset preeclampsia

Project description:Placental Immune alterations in early-onset preeclampsia and late-onset preeclampsia

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Placental Editome Profiling Reveals Widespread RNA-Editing Dysregulation in Preeclampsia

Project description:Dysregulated RNA editing is well documented in several diseases such as cancer. The extent to which RNA editing might be involved in diseases originated in the placenta such as preeclampsia remains unknown, because RNA editing has rarely been studied in the placenta. Here, the RNA editome is systematically profiled on placentae from 9 patients with early-onset severe preeclampsia (EOSPE) and 32 normal controls, and a widespread RNA editing dysregulation in EOSPE has been identified. The mis-edited gene set is enriched with known preeclampsia-associated genes and differentially expressed genes in EOSPE. The “RNA editing events” at two microRNA binding sites in 3’-UTR of the LEP mRNA have been generated, which leads to increased expression level of LEP in trophoblast cells. Upregulation of LEP is also observed in the placentae of PE patients. These results suggest that widespread placental RNA editing may be involved in placental development and dysregulation of RNA editing in the placenta may contribute to the pathogenesis of preeclampsia.

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Transcriptional Profiling of Human Placentas from Pregnancies Complicated by Preeclampsia Reveals Disregulation of Sialic Acid Acetylesterase and Immune Signaling Pathways

Project description:The placenta plays an important role as a regulator of fetal nutrition and growth throughout development and placental factors contribute to gestational abnormalities such as preeclampsia. This study describes the genome-wide gene expression profiles of a large (n=60) set of human placentas in order to uncover gene expression patterns associated with preeclampsia. In addition to confirming changes in expression of soluble factors associated with preeclampsia such as sFLT1 (soluble fms-like tyrosine kinase-1), sENG (soluble endoglin), and INHA (inhibin alpha), we also find changes in immune-associated signaling pathways, offering a potential upstream explanation for the shallow trophoblast invasion and inadequate uterine remodeling typically observed in pathogenesis of preeclampsia. Notably, we also find evidence of preeclampsia-associated placental upregulation of sialic acid acetylesterase (SIAE), a gene functionally associated with autoimmune diseases. 23 preeclamptic, and 37 control placentas included in this study were collected during the years of 2004-2008 and hybridized in two batches to microarrays. Samples were randomized across arrays to control for array and batch variability.

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Molecular subphenotyping using placental transcriptomics in early-onset preeclampsia and fetal growth restriction

Project description:Placental disorders contribute to pregnancy complications including preeclampsia (PE) and fetal growth restriction (FGR), but debate regarding their specific pathobiology persists. Our objective was to apply transcriptomics with weighted gene correlation network analysis (WGCNA) to further clarify the placental dysfunction in these conditions.

2023-08-25 | GSE203507 | GEO

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