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MiRNA seq of feto-placental arterial endothelial cells (pfEC) after normal pregnancy vs pregnancy complicated by gestational diabetes (GDM)

ABSTRACT: miRNA seq of feto-placental arterial endothelial cells (pfEC) after normal pregnancy vs pregnancy complicated by gestational diabetes (GDM)

PROVIDER: PRJNA412262 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6078720.fastq.gz	Fastqsanger.gz
	SRR6078730.fastq.gz	Fastqsanger.gz
	SRR6078721.fastq.gz	Fastqsanger.gz
	SRR6078731.fastq.gz	Fastqsanger.gz
	SRR6078712.fastq.gz	Fastqsanger.gz

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miRNA seq of feto-placental arterial endothelial cells (pfEC) after normal pregnancy vs pregnancy complicated by gestational diabetes (GDM)

Project description:We report that the effect of GDM on gene expression differs between feto-placental endothelial cells of male vs female progeny, i.e. after pregnancy with a male or female offspring.

2019-01-01 | GSE104297 | GEO

Human Feto-placental Arterial and Venous Endothelial Cells are Differentially Programmed by Gestational Diabetes Mellitus Resulting in Cell-specific Barrier Function

Project description:We performed genome-wide methylation analysis of primary feto-placental arterial and venous endothelial cells from healthy (AEC and VEC) and GDM complicated pregnancies (dAEC and dVEC). Parallel transcriptome analysis identified variation in gene expression linked to GDM-associated DNA methylation, implying a direct functional link. Pathway analysis found that genes altered by exposure to GDM clustered to functions associated with ’Cell Morphology’ and ’Cellular Movement’ in both AEC and VEC. Further functional analysis demonstrated that GDM exposed cells have altered actin organization and barrier function. Our data indicate that exposure to GDM programs atypical morphology and barrier function in feto-placental endothelial cells by DNA methylation and gene expression change. The effects differ between AEC and VEC, indicating a stringent cell-specific sensitivity to adverse exposures associated with developmental programming in utero.

2018-08-01 | GSE106099 | GEO

Human Feto-placental Arterial and Venous Endothelial Cells are Differentially Programmed by Gestational Diabetes Mellitus Resulting in Cell-specific Barrier Function Changes

2018-08-01 | GSE103552 | GEO

Plasma protein profiling of women after a GDM pregnancy

Project description:Gestational diabetes (GDM) is a distinctive form of diabetes that first presents in pregnancy. While most women return to normoglycemia after delivery, they are predisposed to an accelerated development of type 2 diabetes. Current prevention strategies remain limited due to our incomplete understanding of the early underpinnings of progression. We therefore examined the protein profiles of women shortly after a GDM pregnancy (using a nested case-control study design within the Study of Women, Infant Feeding and Type 2 Diabetes After GDM Pregnancy) for a comprehensive mechanistic inquiry. At 6-9 weeks postpartum (baseline), differences between women who later developed diabetes (case group) and those who did not (control group) were detected. Notably, protein profiles comprised protease inhibitors, extracellular matrix components, and lipoprotein molecules involved in inflammation. We also identified co-expression networks of differentially altered triglycerides and protein involved in wound healing, highlighting the interplay between dyslipidemia and inflammation. Overall, our findings warrant earlier intervention than previously thought, as defects in postpartum wound healing after a GDM pregnancy, in association with dysmetabolism and insulin resistance, may accelerate type 2 diabetes progression.

2024-09-04 | PXD041243 | Pride

Pigment epithelium derived factor (PEDF): a novel trophoblast derived factor limiting feto-placental angiogenesis in late pregnancy

Project description:We hypothesized that the trophoblast secretes anti-angiogenic factors, which increase in late pregnancy to limit angiogenesis. Therefore, we determined the paracrine effect of primary human trophoblasts from early versus late pregnancy on the angiogenic potential of isolated feto-placental endothelial cells. We found that the expression and secretion of anti-angiogenic factors differs in early vs late pregnancy, and differentially affects feto-placental angiogenesis.

2017-01-01 | GSE69086 | GEO

NRF2 deficiency leads to inadequate beta cell adaptation during pregnancy and gestational diabetes

Project description:The late stages of mammalian pregnancy are accompanied by a mild increase in insulin resistance likely due to enhanced glucose demand of the growing fetus. Therefore, as an adaptive process to maintain euglycemia during pregnancy, maternal β-cell mass expands leading to increased insulin release. Defects in functional β-cell adaptive expansion during pregnancy can lead to gestational diabetes mellitus (GDM). While the exact mechanisms that promote GDM are poorly understood, GDM is associated with inadequate functional β-cell mass expansion and with a systematic increase of oxidative stress. Here, we show that NRF2 levels are upregulated in mouse β-cells at gestational day 15 (GD15). Inducible β-cell-specific Nrf2 deleted (βNrf2KO) mice display reduced β-cell proliferation, increased β-cell oxidative stress and lipid peroxidation, compromised β-cell function, and elevated β-cell death, leading to impaired β-cell mass expansion and dysregulated glucose homeostasis towards the end of pregnancy. Importantly, the gestational hormone 17-β-estradiol (E2) increases NRF2 levels, and downregulation of NRF2 suppresses E2-induced protection of β-cells against oxidative stress, suggesting that E2 exerts its antioxidant effects through activation of NRF2 signaling in β-cells. Collectively, these data highlight the critical role of NRF2 in regulating oxidative stress during the adaptive response of β-cells in pregnancy and identify NRF2 as a potential therapeutic target for GDM treatment.

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Gestational diabetes mellitus alters placental structure, efficiency, and plasticity

Project description:The hemochorial placenta provides a critical barrier at the maternal-fetal interface to modulate maternal immune tolerance and enable gas and nutrient exchange between mother and conceptus. Pregnancy outcomes are adversely affected by gestational diabetes mellitus (GDM); however, the effects of GDM on placental formation, and subsequently fetal development, are not fully understood. In this report, streptozotocin was used to induce hyperglycemia in pregnant rats for the purpose of investigating the impact of GDM on placental formation and fetal development. GDM caused placentomegaly and placenta malformation, decreasing placental efficiency and fetal size. Elevated glucose disrupted rat trophoblast stem (TS) cell differentiation in vitro. Evidence of altered trophoblast differentiation was also observed in vivo, as hyperglycemia affected the junctional zone transcriptome and interfered with intrauterine trophoblast invasion and uterine spiral artery remodeling. When exposed to hypoxia, rats with GDM showed decreased proliferation and ectoplacental cone development on gestation day (gd) 9.5 and complete pregnancy loss by gd 13.5. Furthermore, elevated glucose concentrations inhibited TS cell responses to hypoxia in vitro. Overall, these results indicate that alterations in placental development, efficiency, and plasticity could contribute to the suboptimal fetal outcomes in offspring from pregnancies complicated by GDM.

2020-07-07 | GSE144276 | GEO

EV-microRNA Signatures in Pregnant Women with Idiopathic Recurrent Pregnancy Loss: Deciphering MicroRNAome Pathway Networks at Feto-Maternal Interface

Project description:Despite extensive research in the past decade, the exact pathogenesis of recurrent pregnancy loss (RPL) remains unknown. At the time of pregnancy, human placenta releases microRNAs (miRNAs) enclosed in extracellular vesicles (EVs), which enter into maternal circulation and play an important role at feto-maternal interface to sustain a successful pregnancy. Aberrant expression of these miRNAs often results in adverse pregnancy complications. Therefore, studying the expression of these EV-miRNAs in maternal circulation could provide insights into the pathogenesis of RPL. miRNA sequencing revealed 66 (44 known and 22 novel) significantly DE miRNAs between RPL and healthy pregnant women.

2025-05-07 | GSE296460 | GEO

RNA sequence of gestational diabetes mellitus (GDM) and healthy control placentas

Project description:GDM is a multi-system disorder that is primarily characterised by new-onset hypertension accompanied by proteinuria during gestation. This disease is one of the leading causes of maternal and perinatal morbidity and mortality. In this work, placental samples were collected from GDM and control patients. RNA-seq was performed to identify differences in gene expression. Significantly differentially expressed genes between the GDM and control samples included 64 up-regulated and 296 down-regulated genes. This study may provide further insight in the mechanisms of GDM and function as preventive, predictive and therapeutic measures.

2021-12-31 | GSE154414 | GEO

Plasma exosomal microRNAs associated with metabolism as early predictor of gestational diabetes mellitus

Project description:The microRNA (miRNA) expression profile of plasma exosome in pregnant women complicated with gestational diabetes mellitus (GDM) has not been fully clarified. In this study, differentially expressed miRNAs in plasma exosomes were identified by high-throughput small RNA sequencing in 12 GDM and 12 normal glucose tolerance (NGT) pregnant women and validated in 102 GDM and 101 NGT pregnant women. A total of 22 exosomal miRNAs were found and five of them were verified by qRT-PCR. Exosomal miR-423-5p was upregulated, while miR-99a-5p, miR-192-5p, miR-148a-3p, and miR-122-5p were downregulated in pregnant women complicated with GDM.

2022-11-09 | GSE192813 | GEO

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