Intrauterine inflammation-induced transcriptome changes in the mouse placenta
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ABSTRACT:
PROVIDER: PRJNA637059 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11918624_1.fastq.gz | Fastqsanger.gz | |||
| SRR11918624_2.fastq.gz | Fastqsanger.gz | |||
| SRR11918625_1.fastq.gz | Fastqsanger.gz | |||
| SRR11918625_2.fastq.gz | Fastqsanger.gz | |||
| SRR11918626_1.fastq.gz | Fastqsanger.gz |
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Project description:Placental insufficiency is implicated in the intrauterine infection-associated spontaneous preterm birth. Using a mouse model of LPS-induced intrauterine inflammation that leads to preterm delivery, RNA-seq study was performed in the placenta at gestational day 17 to assess the transcriptome changes.
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Project description:Placental insufficiency is implicated in spontaneous preterm birth (SPTB) associated with intrauterine inflammation. We hypothesized that intrauterine inflammation leads to deficits in the capacity of the placenta to maintain bioenergetic and metabolic stability during pregnancy ultimately resulting in SPTB. Using a mouse model of intrauterine inflammation that leads to preterm delivery, we performed RNA-seq and metabolomics studies to assess how intrauterine inflammation alters gene expression and/or modulates metabolite production and abundance in the placenta. 1871 differentially expressed genes were identified in LPS-exposed placenta. Among them, 1,149 and 722 transcripts were increased and decreased, respectively. Ingenuity pathway analysis showed alterations in genes and canonical pathways critical for regulating oxidative stress, mitochondrial function, metabolisms of glucose and lipids, and vascular reactivity in LPS-exposed placenta. Many upstream regulators and master regulators important for nutrient-sensing and mitochondrial function were also altered in inflammation exposed placentae, including STAT1, HIF1α, mTOR, AMPK, and PPARα. Comprehensive quantification of metabolites demonstrated significant alterations in the glucose utilization, metabolisms of branched-chain amino acids, lipids, purine and pyrimidine, as well as carbon flow in TCA cycle in LPS-exposed placenta compared to control placenta. The transcriptome and metabolome were also integrated to assess the interactions of altered genes and metabolites. Collectively, significant and biologically relevant alterations in the placenta transcriptome and metabolome were identified in placentae exposed to intrauterine inflammation. Altered mitochondrial function and energy metabolism may underline the mechanisms of inflammation-induced placental dysfunction.
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Project description:The placenta has a critical role in fetal growth, with many key functions regulated by genomic imprinting. With the recent description of polymorphic placenta-specific imprinting, the molecular mechanisms leading to this curious epigenetic phenomenon are unknown, as is their involvement in pregnancies complications. Profiling ubiquitous and placenta-specific imprinted differentially methylated regions (DMRs) exposed isolated aberrant methylation at ubiquitous DMRs as well as abundant hypomethylation at placenta-specific DMRs. Analysis of underlying chromatin at polymorphic placenta-specific imprinted DMRs revealed biallelic enrichment of histone H3K4 methylation, a modification normally mutually exclusive with DNA methylation. Furthermore, characterisation of expression in intrauterine growth restricted samples (IUGRs) uncovered coordinated deregulation of the GPR1AS1-ZDBF2-ADAM23 locus. Our results emphasize that methylation is less stable at placenta-specific imprints compared to their ubiquitous counterparts and that further work is required to determine if these differences are the IUGR cause or reflect unique adaption of the placenta epigenome to developmental stresses.
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Project description:Gestational diabetes mellitus (GDM) with intrauterine hyperglycemia induces a series of changes in the placenta, which have adverse effects on both the mother and fetus. Although some studies have examined these changes in the placenta, the differences resulting from fetal sex remain unelucidated. In this study, we established an intrauterine hyperglycemic model using ICR mice. We collected placental specimens before birth for histological observation using Hematoxylin and Eosin (HE) staining, along with Tandem Mass Tag (TMT) labeled proteomic analysis which was stratified by sex. In both male and female fetuses of the GDM group, body weight and placental weight were significantly lower compared to the control group. Additionally, the placenta-to-body weight ratio was higher, suggesting potential placental insufficiency. Histological analysis revealed smaller sizes and reduced thickness of the junctional zone and labyrinth in diabetic placentas at E18.5, along with ectopic accumulation of spongiotrophoblasts in the labyrinth. When the analysis was not segregated by sex, the GDM group showed 208 upregulated and 225 downregulated proteins in the placenta, primarily within the extracellular matrix and mitochondria. Altered biological processes included cholesterol metabolism and oxidative stress responses. After stratifying by sex, the male subgroup displayed 209 upregulated and 111 downregulated proteins, while the female subgroup exhibited 97 upregulated and 75 downregulated proteins. Among these, 64 differentially expressed proteins showed consistent trends across both sexes, primarily enriched in the JAK-STAT signaling pathway, complement and coagulation cascades, and metabolism-related modifications. The male subgroup showed a heightened tendency for immune-related pathway alterations, whereas the female subgroup manifested changes in branched-chain amino acid metabolism. The intrauterine hyperglycemic environment affects both placental morphology and proteomics, leading to shifts in energy metabolism, oxidative stress responses, and immune processes. Our study suggests that the observed differences in placental protein expression specific to each sex may provide an explanation for the varying impacts of GDM on offspring.
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Project description:Intrauterine growth restriction (IUGR) is a serious pathological complication associated with compromised fetal development during pregnancy. The aim of the study was to broaden knowledge about the transcriptomic complexity of the human placenta by identifying genes potentially involved in IUGR pathophysiology. RNA-Seq data were used to profile protein-coding genes, detect alternative splicing events (AS), single nucleotide variant (SNV) calling, and RNA editing sites prediction in IUGR-affected placental transcriptome. The applied methodology enabled detection of 37,501 transcriptionally active regions and the selection of 28 differentially-expressed genes (DEGs), among them 10 were upregulated and 18 downregulated in IUGR-affected placentas. Functional enrichment annotation indicated that most of the DEGs were implicated in the processes of inflammation and immune disorders related to IUGR and preeclampsia. Additionally, we revealed that some genes (S100A13, GPR126, CTRP1, and TFPI) involved in the alternation of splicing events were mainly implicated in angiogenic-related processes. Significant SNVs were overlapped with 6533 transcripts and assigned to 2386 coding sequence (CDS), 1528 introns, 345 5' untranslated region (UTR), 1260 3'UTR, 918 non-coding RNA (ncRNA), and 10 intergenic regions. Within CDS regions, 543 missense substitutions with functional effects were recognized. Two known mutations (rs4575, synonymous; rs3817, on the downstream region) were detected within the range of AS and DEG candidates: PA28β and PINLYP, respectively. Novel genes that are dysregulated in IUGR were detected in the current research. Investigating genes underlying the IUGR is crucial for identification of mechanisms regulating placental development during a complicated pregnancy.
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