Ontology highlight
ABSTRACT:
PROVIDER: PRJNA471333 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7163580_1.fastq.gz | Fastqsanger.gz | |||
| SRR7163580_2.fastq.gz | Fastqsanger.gz | |||
| SRR7163590_1.fastq.gz | Fastqsanger.gz | |||
| SRR7163590_2.fastq.gz | Fastqsanger.gz | |||
| SRR7163600_1.fastq.gz | Fastqsanger.gz |
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Project description:Introduction: Air pollution is detrimental to a pregnancy with adverse effects in mother and child. It is also known to increase pregnancy complications including risk factors of gestational diabetes. Methods: We investigated the impact of intra-nasal instilled air pollutants upon gestational day 16-19 maternal mouse cardiovascular and metabolic status, placental nutrient transporters, and placental-fetal size and morphology. To further unravel mechanisms, we also examined placental total DNA 5’-hydroxymethylation and bulk RNA sequenced gene expression profiles. Results: Air pollution exposed pregnant mice were tachycardic, hyperglycemic, glucose intolerant and insulin resistant, with no major placental glucose and fatty acid transporter changes, except for a spatial disruption of cells expressing GLUT10 that imports L-dehydroascorbic acid in protecting against oxidative stress. Placentas revealed inflammatory cellular infiltration with associated cellular edema and necrosis, with a paucity of vascularity and hemorrhage. While individual fetal body weights increased, they suffered a reduction in brain cortical thickness. Placental total DNA 5’-hydroxymethylation was 2.5-fold higher, with perturbed gene expression profiles involving key metabolic, inflammatory, transcriptional, cellular polarizing and processing genes and pathways. Discussion: We conclude that gestational exposure to air pollutants incites a maternal inflammatory response resulting in features of maternal gestational diabetes mellitus with altered placental gene expression with associated injury to the placental-fetal unit. Thus, air pollutants adversely impact the health of mother and offspring.
2025-03-07 | GSE261095 | GEO
Project description:We performed the single cell RNAsequencing in the placental tissues of term pregnancies with gestational diabetes mellitus complicated with macrosomia after cesarean section to explore the transcriptome differences and potential mechanisms of placenta in the process of macrosomia in patients with gestational diabetes. Our research helps to understand placental overgrowth in GDMM and its impact on fetal development, providing new insights into the pathogenesis of GDMM and predicting potential therapeutic interventions.
2025-04-16 | GSE267340 | GEO
Project description:Placental ageing refers to the physiological accumulation of a senescent phenotype over healthy pregnancy. In pregnancies affected by complications such as pre-eclampsia and fetal growth restriction, placental ageing is notably accelerated and observed at an earlier gestational age. Metformin is used during pregnancy for an increasing variety of indications, including treatment of gestational diabetes and may have a role in slowing cellular ageing. It is therefore essential to understand the potential impact of metformin on placental ageing. Placental samples (n=105) were obtained from women with BMI ≥30kg/m2 randomised to treatment with metformin or placebo during pregnancy. Ageing was assessed by measuring telomere length, histological examination, and using array-based technologies to investigate gene expression and methylation. Results were validated using isolated human trophoblasts treated in vitro with metformin, and in a complementary mouse model. There were no differences between metformin-exposed and control placentas in terms of telomere length, fibrosis, or calcification. There were no differences in placental gene expression or methylation patterns by metformin status. In our mouse model, no genes classically associated with cellular ageing were differentially expressed and no senescence pathway showed evidence of enrichment with metformin treatment. There was no evidence that metformin either slows or accelerates placental ageing pathways in the complementary models that we investigated. Our findings are reassuring with regards to the safety of metformin used to treat gestational diabetes, but do not support a role for metformin in the prevention of adverse pregnancy outcomes in non-diabetic women.
2025-06-18 | GSE293162 | GEO
Project description:BACKGROUND: Although gestational diabetes affects up to 10% of all pregnancies, there is ambiguity as to whether the disease subtype classifications are biologically significant at the maternal-fetal interface, or more reflective of an extended spectrum of normal pregnancy endocrine physiology. OBJECTIVE: Bulk RNA-sequencing (RNA-seq), single-cell RNA-sequencing (scRNA-seq), and spatial transcriptomics have been integrated to reveal gene signatures of disease in subsets of cells and microenvironments. We aimed to combine these high-resolution technologies with rigorous classification of diabetes subtypes in pregnancy. We hypothesized that differences between pre-existing and gestational diabetes subtypes would be associated with altered gene expression profiles in specific placental cell populations. STUDY DESIGN: In a two-phase case-cohort design, we clinically validated gestational diabetes mellitus type 1 (GDMA1), GDMA2, and type 2 diabetes (T2DM) cases within a cohort of placentae and compared them to healthy controls by bulk RNA-seq (n=54). Quantitative analysis with RT-qPCR of presumptive genes of significant interest were undertaken in an independent and non-overlapping validation cohort of similarly well-characterized cases and controls (n=122). Additional integrated analyses of term placenta single-cell, single-nuclei, and spatial transcriptomics data to determine the cellular subpopulations and niches that aligned with the GDMA1, GDMA2, and T2DM gene expression signatures. RESULTS: Dimension reduction of the bulk RNA-seq data revealed that the most common source of placental gene expression variation was diabetic disease subtype. Relative to controls, we found 2,052 unique significantly differentially expressed transcripts (-2<Log2(fold-change)>2 threshold; q<0.05 Wald Test) among GDMA1 placental specimens, 267 among GDMA2, and 1,520 among T2DM. Several candidate marker genes (CSH1, PER1, PIK3CB, FOXO1, EGFR, IL2RB, SOD3, DOCK5, and SOGA1) were validated in an independent and non-overlapping validation cohort (q<0.05 Tukey). Functional enrichment revealed the pathways and genes most impacted for each diabetes subtype, and degree of proximal similarity to other subclassifications. Surprisingly, GDMA1 and T2DM were more proximal by virtue of increased expression of chromatin remodeling and epigenetic regulation genes, while albumin was the top marker for GDMA2 with increased expression of genes in the wound healing pathway. Assessment of these gene signatures in the single-cell, single-nuclei, and spatial transcriptomics data revealed expression of these genes were highly variable by placental cell and microarchitecture type. For example, at the cellular and spatial (e.g., microarchitectural) levels, distinguishing features were observed in in extravillous trophoblasts (GDMA1) and macrophages (GDMA2). Lastly, we utilized these data to generate machine learning models to predict participants diabetes status and observed greater proximity of placental gene expression among GDMA1 and T2DM participants relative to GDMA2. CONCLUSION: Consistent with their distinct risks of perinatal outcomes, placentae from GDMA1, GDMA2, and T2DM affected pregnancies harbor gene signatures which can be further distinguished by placental microarchitecture and cellular subtypes.
2025-05-05 | GSE249311 | GEO
Project description:The placenta is a potent endocrine organ that secretes hormones with metabolic effects into maternal circulation. On the other hand, the liver, which is the main detoxification organ of the body, plays a key role in regulating maternal glucose and insulin metabolism during pregnancy. Failures in the production of placental hormones and/or the liver to adapt its structure and function to pregnancy can result in metabolic diseases such as gestational diabetes. Previous work has shown that the imprinted Igf2-H19 locus is involved in controlling placental endocrine function in mice. This study used conditional mis-expression of the Igf2-H19 locus to induce placental endocrine malfunction and study its consequences on hepatic gene regulation during pregnancy.
2024-11-27 | E-MTAB-11439 | biostudies-arrayexpress
Project description:The objective of this study was to investigate whether placental exosomes in gestational diabetes mellitus (GDM) carries a specific set of miRNAs associated with skeletal muscle insulin sensitivity. Exosomes were isolated from chorionic villi-conditioned media and plasma from normal and GDM pregnancies. A specific set of miRNAs was identified to be selectively enriched within exosomes when compared to their cells of origin indicating specific packaging of miRNAs into exosomes. In addition, miRNA expression varies in a consistent pattern in placenta, placental-derived exosomes, circulating exosomes and skeletal muscle in GDM.
2021-03-20 | GSE112168 | GEO
Project description:Gestational diabetes mellitus alters placental structure, efficiency, and plasticity
| PRJNA603282 | ENA
Project description:Pancreatic β-cell function impairment is a key mechanism for developing gestational diabetes mellitus (GDM). Maternal and placental exosomes regulate maternal and placental responses during hyperglycemia. Studies have associated exosomal micro RNAs (miRNAs) with GDM development. To date, no studies have been reported that evaluate the profile of miRNAs present in maternal and placental exosomes in the early stages of gestation from pregnancies that develop GDM. We used microarrays to assess whether early pregnancy maternal and placental exosomal miRNA profiles vary according to pancreatic β-cell function in women who will develop GDM (preGDM).
2024-02-29 | GSE243374 | GEO
Project description:Gestational diabetes is a common medical complication of pregnancy that is associated with adverse perinatal outcomes and an increased risk of metabolic diseases and atherosclerosis in adult offspring. The mechanisms responsible for this delayed pathological transmission remain unknown. In mouse models, we found that the development of atherosclerosis in adult offspring born to diabetic pregnancy can be in part linked to hematopoietic alterations. Although they do not show any gross metabolic disruptions, the adult offspring maintain hematopoietic features associated with diabetes, indicating the acquisition of a lasting diabetic hematopoietic memory. We show that the induction of this hematopoietic memory during gestation relies on the activity of the pattern recognition receptor AGER and the NLRP3 inflammasome, which leads to increased placental inflammation. In adult offspring, we find that this memory is associated with DNMT1 upregulation and epigenetic changes in hematopoietic progenitors. Altogether, our results demonstrate that the hematopoietic system can acquire a lasting memory of gestational diabetes, and that this memory constitutes a new pathway connecting gestational health to adult pathologies.
2023-11-13 | GSE244688 | GEO
Project description:Data on the temporal dynamics of human placental gene expression is scarce. We have completed the first whole-genome profiling of human placental gene expression dynamics (GeneChips, Affymetrix®) from early to mid- gestation (10 samples; gestational weeks 5 to 18) and report 154 genes with considerable change in transcript levels (FDR P<0.1). Functional enrichment analysis revealed >200 GO categories that are statistically over-represented among 105 genes with dynamically increasing transcript levels. Analysis in an extended sample (n=43; gestational weeks 5 to 41) conformed a highly significant (FDR P<0.05) expressional peak in mid-gestation placenta for ten genes: BMP5, CCNG2, CDH11, FST, GATM, GPR183, ITGBL1, PLAGL1, SLC16A10, STC1. A central hypothesis of our study states that the aberrant expression of genes characteristic to mid-gestation placenta may contribute to affected fetal growth, maternal preeclampsia (PE) or gestational diabetes (GD). The gene STC1 coding for Stanniocalcin 1 (STC1) was identified with a sharp placental expressional peak in mid-gestation, increased mRNA levels at term and significantly elevated STC1 protein levels in post-partum maternal plasma in all pregnancy complications. The highest STC1 levels were identified in women, who developed simultaneously PE and delivered an SGA baby (median 731 vs 418 pg/ml in controls; P=0.001). CCNG2 and LYPD6 exhibited significantly increased placental mRNA expression and enhanced intensity of immunohistochemistry staining in placental sections all studied in GD and PE cases. Aberrant expression of mid-gestation specific genes in pregnancy complications at term indicates the importance of the fine-scale tuning of the temporal dynamics of transcription regulation in placenta. Observed significantly elevated plasma STC1 in complicated pregnancies warrants further investigations of its potential as a biomarker. Interestingly, a majority of genes with high expression in mid-gestation placenta have also been implicated in adult complex disease. This observation promotes a recently opened discussion on the role of placenta in developmental programming. 4 samples; this submission is extension of our earlier study (accession GSE22490).
2012-05-10 | E-GEOD-37901 | biostudies-arrayexpress