C8020190-7893-4c54-a74a-6aeea4164ba6 - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001008317 | EGA |
REPOSITORIES: EGA
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Project description:Patients having major surgery experience inflammation post-operatively, which may contribute to post-operative morbidity. Endogenous glucocorticoids (GCs) are an essential part of the stress response, but this response varies between individuals, which may in turn affect clinical outcome in general, and post-operative inflammation, specifically. Exon 1 of the NR3C1 gene, encoding the glucocorticoid receptor, contains an established region of differential regulation. DNA methylation patterns in this region have been found to differ between individuals. We investigated the methylation status and genotype in the Cytosine-phosphate-Guanine (CpG) island in exon 1 of NR3C1 in 24 patients who underwent major abdominal surgery and correlated it with post-operative complications. DNA was extracted from peripheral blood leukocytes and underwent targeted bisulfite sequencing of the CpG island. Complications were graded according to the Clavien-Dindo classification and 14 out of 24 had post-operative complications. Multifactorial and partial least square methods were used to analyse the data. A homogenous demethylated pattern was observed in all patients and no single CpG methylation was associated with post-operative complications. Four single nucleotide polymorphisms (SNPs) were significantly correlated with higher Clavien-Dindo scores. Genetic variability in the chr5:143,402,505-143,405,805 region of exon 1 of the glucocorticoid receptor gene NR3C1, but not DNA methylation, was associated with more severe post-operative complications in patients having major abdominal surgery. This indicates that the response to GCs may be of clinical importance for inflammatory conditions.
| EGAS00001005737 | EGA
Project description:Colorectal cancer (CRC), among the major cancer types in western world is responsible for 10% of cancer related deaths, often due to late detection when the tumor has already spread out of the colon. Surgery is the mainstay curative treatment for CRC. Nevertheless, between 15-30% of stage II and III patients develop hepatic metastasis within 5 years. Paradoxically, tumor surgery can contribute to the metastatic process, due to inflammatory mediator release in response to surgery, which promotes the metastatic ability of cancer cells. During surgery, bacterial products, such as LPS, from commensal bacteria translocate across the bowel wall, reach systemic circulation and induce an inflammatory response through to the activation of the Nuclear Factor-ĸB (NF-ĸB) pathway. Inflammation promotes malignant transformation by inducing chromosomal and microsatellite instability or CpG island methylation [14], but its direct effect on cancer cells and contribution to metastasis development remains to be elucidated. In this experiment we mimic the perioperative microenvironment where bacterial products get in contact with CRC cancer cells. We assessed the identity of the secreted proteins, including those released through extracellular vesicles (EV), of six CRC cell lines once exposed to lipopolysaccharide (LPS).
2022-02-28 | PXD011611 | Pride
Project description:Differential CpG methylation profiling for KMT2D and HNF4A genomic region in pancreatic cancer cells was performed using Illumina MiSeq.
2018-08-20 | GSE85961 | GEO
Project description:Cardiac surgery and cardiopulmonary bypass induce a substantial immune and inflammatory response, the overactivation of which is associated with significant complications. Longitudinal DNA methylation profiling allows the potential to identify changes in gene regulatory mechanisms that are secondary to surgery and to identify molecular processes that predict and/or cause postoperative complications. In this study, we measure DNA methylation in preoperative and postoperative whole blood samples from 96 patients undergoing cardiac surgery on cardiopulmonary bypass. We identify several loci with statistically significant postoperative changes in methylation. Additionally, two of these loci are associated with new-onset postoperative atrial fibrillation, a significant complication after cardiac surgery. This research establishes that there are statistically significant changes in DNA methylation that occur immediately after cardiac surgery and that these acute alterations in DNA methylation have the granularity to identify processes associated with major postoperative complications.
2023-01-09 | GSE215937 | GEO
Project description:Gestational diabetes mellitus (GDM) affects approximately 18% of pregnancies in the United States and increases the risk of adverse health outcomes in the offspring. These adult disease propensities may be set by anatomical and molecular alterations in the placenta associated with GDM. To assess the mechanistic aspects of fetal programming, we measured genome-wide methylation (Infinium HumanMethylation450 Beadchips) and expression (Affymetrix Transcriptome Microarrays) in placental tissue of 41 GDM cases and 41 matched pregnancies without maternal complications from the Harvard Epigenetic Birth Cohort. Specific transcriptional and epigenetic perturbations associated with GDM status included alterations in the major histocompatibility complex (MHC) region, which were validated in an independent cohort, the Rhode Island Child Health Study. Gene ontology enrichment among gene regulation influenced by GDM revealed an over-representation of immune response pathways among differential expression, reflecting these coordinated changes in the MHC region. Our study represents the largest investigation of transcriptomic and methylomic differences associated with GDM, providing comprehensive insight into the molecular basis of GDM induced fetal (re)programming. Bisulphite converted DNA extracted from the placentas (maternal-side) of 41 clinically-confirmed cases of GDM and 41 pregnancies without maternal complications were hybridised to the Illumina Infinium HumanMethylation450 Beadchips
2015-08-03 | E-GEOD-70453 | biostudies-arrayexpress
Project description:20 random DNA barcodes were designed in silico and transfected into PC3 cells. Barcodes were sequenced using Illumina-Miseq technology to find the sequence and their respective copy numbers. Current file contains the raw data of these DNA barcodes in fastq format
2016-03-31 | GSE67441 | GEO
Project description:Gestational diabetes mellitus (GDM) affects approximately 18% of pregnancies in the United States and increases the risk of adverse health outcomes in the offspring. These adult disease propensities may be set by anatomical and molecular alterations in the placenta associated with GDM. To assess the mechanistic aspects of fetal programming, we measured genome-wide methylation (Infinium HumanMethylation450 Beadchips) and expression (Affymetrix Transcriptome Microarrays) in placental tissue of 41 GDM cases and 41 matched pregnancies without maternal complications from the Harvard Epigenetic Birth Cohort. Specific transcriptional and epigenetic perturbations associated with GDM status included alterations in the major histocompatibility complex (MHC) region, which were validated in an independent cohort, the Rhode Island Child Health Study. Gene ontology enrichment among gene regulation influenced by GDM revealed an over-representation of immune response pathways among differential expression, reflecting these coordinated changes in the MHC region. Our study represents the largest investigation of transcriptomic and methylomic differences associated with GDM, providing comprehensive insight into the molecular basis of GDM induced fetal (re)programming. RNA extracted from the placentas (maternal-side) of 30 clinically-confirmed cases of GDM and 25 pregnancies without maternal complications was hybridised to the GeneChip® Human Transcriptome Array 2.0 (Affymetrix). Four samples were run in triplicate.
2015-08-03 | E-GEOD-70493 | biostudies-arrayexpress
Project description:In mouse development, long-term silencing by CpG island DNA methylation is specifically targeted to germline genes, however the molecular mechanisms of this specificity remain unclear. Here we demonstrate that the transcription factor E2F6, a member of the polycomb repressive complex 1.6 (PRC1.6), is critical to target and initiate epigenetic silencing at germline genes in early embryogenesis. Genome-wide, E2F6 binds preferentially to CpG islands in embryonic cells. E2F6 cooperates with MGA to silence a subgroup of germline genes in mouse embryonic stem cells and in vivo, a function that critically depends on the E2F6 marked box domain. Inactivation of E2f6 leads to a failure to deposit CpG island DNA methylation at these genes during implantation. Furthermore, E2F6 is required to initiate epigenetic silencing in early embryonic cells but becomes dispensable for the maintenance in differentiated cells. Our findings elucidate the mechanisms of epigenetic targeting of germline genes and provide a paradigm for how transient repression signals by DNA-binding factors in early embryonic cells are translated into long term epigenetic silencing during mammalian development.
2021-04-22 | PXD023974 | Pride
Project description:Purpose: Our previous study has confirmed that reduction of SIRT3 expression is a main factor contributing to salt-induced hepatic inflammtion. Here we sought to investigate whether salt-induced SIRT3 reduction was related to epigenetic modification. Methods: 6-week-old male wild-type mice were fed with high salt diet (HSD, containing 8% NaCl) or normal salt diet (NSD, containing 0.4% NaCl) for 4 months. And then their liver tissues were removed and subjected to bilsulfate-seq. Results: Through bisulfate-seq, we did not observe any change in DNA methylation in the CpG island of Sirt3 gene promoter region. Conclusions: Salt-induced SIRT3 reduction is not related to DNA methylation on SIRT3 gene promoter.
2023-09-01 | GSE183583 | GEO