Effects of intrauterine hyperglycemia on offspring development in gestational diabetes mellitus based on placental transcriptomics
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE263483 | GEO | 2024/07/30
REPOSITORIES: GEO
Similar Datasets
Project description:To investigate the umbilical cord lncRNA profiles in gestational diabetes-induced macrosomia, the umbilical cord vein blood from normal and gestational diabetes-induced macrosomia was hybridized to a microarray containing probes representing 33,000 lncRNA genes. Quantitative real-time polymerase chain reaction (qPCR) was used to validate selected differentially expressed lncRNAs. The gene ontology (GO), pathway and network analysis were performed. The microarray identified 8814 lncRNAs that were expressed in the umbilical cord blood, of which 349 were significantly upregulated and 892 were significantly downregulated (fold-change M-bM-^IM-% 2.0) in GDM group. The highest enriched GOs targeted by downregulated transcripts were biological regulation. Pathway analysis indicated that nine pathways corresponded to downregulated transcripts. Thirty pairs of GDM macrosomia and normal controls were divided into three subgroups randomly, and the umbilical cord vein blood from each subgroup was mixed, and hybridized to a microarray.
2015-02-25 | E-GEOD-65737 | biostudies-arrayexpress
Project description:Genomic expression profiles of blood and placenta reveal significant immune-related pathways and categories in Chinese women with Gestational Diabetes Gestational diabetes mellitus (GDM) is a complex metabolic disease which occurs in pregnancy with high prevalence, and its pathogenesis remains elusive. Thus far, there has been no comprehensive gene expression profiling in Chinese women with GDM. In this study, we attempt to define the genes and/or pathways that are involved in GDM with Chinese ethnicity, by the Illumina microarray technique. We found 5,197 and 243 genes with significantly altered expression due to GDM in blood and placenta tissues, respectively. Previously known genes (such as TNF, IL1B, LEP, IFNG, and HLA-G) with altered gene expression in GDM were also validated here. In addition, we identified undescribed genes VAV3, PTPN6, CD48 and IL15, in which expression was related to GDM by microarray and Q-RT-PCR assays. To identify GDM-associated pathways, we used analyses with integrated functional annotation (i.e. KEGG) and extracted two significant pathways, which were Natural killer cell mediated cytotoxicity (hsa04650; FDR = 7.10E-09) in blood and Cytokine-cytokine receptor interaction (hsa04060; FDR = 1.07E-03) in placenta tissues. Immune system process (GO: 0002376) was identified by GO analysis with FDR P-value = 7.01E-60 in blood and FDR P-value = 3.57E-08 in placenta tissues, indicating the importance of immunological and inflammatory categories in GDM. Furthermore, despite differences in the quantity of gene expression, we observed a similar functional distribution between expression of blood and placenta tissues in GDM under the categories of immunity. These newly identified key genes and pathways may provide valuable information for the pathogenesis of GDM and advance disease diagnosis, prevention, medication design, and clinical treatment of the disease. One individual GDM blood tissue sample and one pooled GDM blood tissue sample were compared to one pooled healthy blood tissue sample. One pooled GDM placenta tissue sample was compared to one pooled healthy placenta tissue sample.
2010-12-23 | E-GEOD-19649 | biostudies-arrayexpress
Project description:Exosomes are the smallest extracellular vesicles which are released during pregnancy by the placenta, umbilical cord, amniotic fluid and various cell membranes in the extracellular space. The content of exosomes during pregnancy is strongly related to various conditions such as gestational diabetes mellitus (GDM). Although it is well-known that GDM is characterized by different levels of chronic low-grade inflammation, complement system dysregulation, vascular dysfunction and platelet activation, there is little data characterizing the serum exosomal protein cargo of GDM patients and their associations to these processes. The aim of this study was to analyze the serum exosomal proteome of GDM patients, with focus on the platelet activation and the complement proteins and their relationship to serum biochemical parameters and other protein markers of lipid metabolism and prothrombotic factors.
2022-09-22 | PXD035673 | Pride
Project description:Exosomal RNAs in cord blood may allow intercellular communication between maternal and fetus. We aimed to establish exosomal RNA expression profiles in cord blood exosomes from gestational diabetes mellitus (GDM) patients with macrosomia.We used microarray technology to establish the differential mRNA, lncRNA and circRNA expression profiles in cord blood exosomes from GDM patients with macrosomia compared with normal controls. A total of 98 mRNAs, 372 lncRNAs and 452 circRNAs were differentially expressed in cord blood exosomes from GDM patients with macrosomia. Pathway analysis showed the differential genes were associated with PI3K-Akt signaling pathway, JAK-STAT signaling pathway, TGF-beta signaling pathway, insulin resistance, glycerolipid metabolism, fatty acid degradation and mTOR signaling pathway. These results showed that exosomal RNAs are aberrantly expressed in the cord blood of GDM patients with macrosomia.
2022-01-21 | GSE194119 | GEO
Project description:A physiological state of insulin resistance is required to preferentially direct maternal nutrients toward the feto-placental unit, allowing adequate growth of the fetus. When women develop gestational diabetes mellitus (GDM), insulin resistance is more severe and disrupts the intrauterine milieu, resulting in accelerated fetal development with increased risk of macrosomia. As a natural interface between mother and fetus, the placenta is the obligatory target of such environmental changes. However, the molecular basis for the imbalance that leads to fetal, neonatal, and adult metabolic compromises is not well understood. We report that GDM elicits major changes in the expression profile of placental genes with a prominent increase in markers and mediators of inflammation. Within the 435 transcripts reproducibly modified, genes for stress-activated and inflammatory responses represented the largest functional cluster (18.5% of regulated genes). Upregulation of interleukins, leptin, and tumor necrosis factor-{alpha} receptors and their downstream molecular adaptors indicated an activation of pathways recruiting stress-activated protein/c-Jun NH2-terminal kinases. Transcriptional activation of extracellular matrix components and angiogenic activators pointed to a major structural reorganization of the placenta. Thus, placental transcriptome emerges as a primary target of the altered environment of diabetic pregnancy. The genes identified provide the basis to elucidate links between inflammatory pathways and GDM-associated insulin resistance. Keywords: other
2005-07-18 | GSE2956 | GEO
Project description:Studies on human and animals suggest associations between gestational diabetes mellitus (GDM) with impaired cognitive performance in offspring. Using a mouse model of diabetes during pregnancy, we found that intrauterine hyperglycemia exposure resulted in memory impairment in both the first filial (F1) males and the second filial (F2) males from the F1 male offspring. The effects of intrauterine hyperglycemia exposure on F1 and F2 hippocampus gene expression were also examined.
2021-08-25 | GSE147039 | GEO
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
Project description:Gestational diabetes mellitus (GDM), the most prevalent metabolic disorder during pregnancy, has long-term risks of metabolic diseases that might persist in adulthood. However, the underlying mechanisms remain unclear. Here, we profiled 78,767 cord blood mononuclear cells (CBMCs) from GDM and healthy mothers’ fetuses by single-cell RNA sequencing (scRNA-seq).
2024-01-18 | GSE212309 | GEO
Project description:Genomic expression profiles of blood and placenta reveal significant immune-related pathways and categories in Chinese women with Gestational Diabetes Gestational diabetes mellitus (GDM) is a complex metabolic disease which occurs in pregnancy with high prevalence, and its pathogenesis remains elusive. Thus far, there has been no comprehensive gene expression profiling in Chinese women with GDM. In this study, we attempt to define the genes and/or pathways that are involved in GDM with Chinese ethnicity, by the Illumina microarray technique. We found 5,197 and 243 genes with significantly altered expression due to GDM in blood and placenta tissues, respectively. Previously known genes (such as TNF, IL1B, LEP, IFNG, and HLA-G) with altered gene expression in GDM were also validated here. In addition, we identified undescribed genes VAV3, PTPN6, CD48 and IL15, in which expression was related to GDM by microarray and Q-RT-PCR assays. To identify GDM-associated pathways, we used analyses with integrated functional annotation (i.e. KEGG) and extracted two significant pathways, which were Natural killer cell mediated cytotoxicity (hsa04650; FDR = 7.10E-09) in blood and Cytokine-cytokine receptor interaction (hsa04060; FDR = 1.07E-03) in placenta tissues. Immune system process (GO: 0002376) was identified by GO analysis with FDR P-value = 7.01E-60 in blood and FDR P-value = 3.57E-08 in placenta tissues, indicating the importance of immunological and inflammatory categories in GDM. Furthermore, despite differences in the quantity of gene expression, we observed a similar functional distribution between expression of blood and placenta tissues in GDM under the categories of immunity. These newly identified key genes and pathways may provide valuable information for the pathogenesis of GDM and advance disease diagnosis, prevention, medication design, and clinical treatment of the disease.
2010-12-23 | GSE19649 | GEO
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