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DNA methylation variability in a pilot study group with ischemic stroke

ABSTRACT: Elevated plasma homocysteine is an independent risk factor for cardiovascular disease and stroke, however the etiology remains poorly understood. Elevated homocysteine is known to inhibit methyltransferases including DNA methyltransferases, but no methylome-wide analysis of elevated homocysteine has been reported. Peripheral blood genomic DNA methylation in 8 Singaporean-Chinese ischemic stroke patients (4 male, 4 female) with varying homocysteine titer and hypertensive status were profiled using methyl-CpG binding domain (MBD) protein-enriched genome sequencing (MBD-seq) on Illumina Genome Analyzer IIx. A methylome wide screen was undertaken for gender, total plasma homocysteine, hypertension and age. The data show considerable variability within the small cohort, including at genes which are related to one carbon metabolism and cardiovascular disease.

ORGANISM(S): Homo sapiens

PROVIDER: GSE57962 | GEO | 2014/05/27

SECONDARY ACCESSION(S): PRJNA248568

REPOSITORIES: GEO

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DNA methylation variability in a pilot study group with ischemic stroke

Project description:Elevated plasma homocysteine is an independent risk factor for cardiovascular disease and stroke, however the etiology remains poorly understood. Elevated homocysteine is known to inhibit methyltransferases including DNA methyltransferases, but no methylome-wide analysis of elevated homocysteine has been reported. Peripheral blood genomic DNA methylation in 8 Singaporean-Chinese ischemic stroke patients (4 male, 4 female) with varying homocysteine titer and hypertensive status were profiled using methyl-CpG binding domain (MBD) protein-enriched genome sequencing (MBD-seq) on Illumina Genome Analyzer IIx. A methylome wide screen was undertaken for gender, total plasma homocysteine, hypertension and age. The data show considerable variability within the small cohort, including at genes which are related to one carbon metabolism and cardiovascular disease. Peripheral blood genomic DNA methylation in 8 Singaporean-Chinese ischemic stroke patients (4 male, 4 female) was profiled using methyl-CpG binding domain (MBD) protein-enriched genome sequencing (MBD-seq) on Illumina Genome Analyzer IIx. Methylation parrterns were correlated with homocysteine levels, lypertensive status, gender and age.

2014-05-27 | E-GEOD-57962 | biostudies-arrayexpress

The effect of homocysteine on human aortic smooth muscle cells

Project description:Vascular calcification is a common manifestation of atherosclerosis and involves cell-mediated processes similar to the formation of bone (osteogenesis). Elevated plasma levels of homocysteine are an independent risk factor for atherosclerotic vascular disease but the underlying mechanisms remain unclear. We postulated that hcy can modulate the cells involved in atherosclerosis to promote calcification. Cell experiments were performed to assess the effect of homocysteine on the osteogenic differentiation of aortic smooth muscle cells (AoSMC). Keywords: dose repsonse comparison To study the ability of homocysteine to induce osteogenic differentiation, AoSMC were cultured in T75 flasks (7.5x10E5 /mL) in growth medium with 0, 10 and 100 μmol/L DL-homocysteine. Four biological replicates were prepared for each condition. After 14 days, RNA was extracted from cells and the expression levels of osteogenic genes were compared between the different conditions of homocysteine concentration.

2008-10-21 | E-GEOD-9490 | biostudies-arrayexpress

Homocysteine induced alterations in gene expression in neural crest cells

Project description:The amino acid homocysteine increases in the serum when there is insufficient folic acid or vitamin B12, or with certain mutations in enzymes important in methionine metabolism. Elevated homocysteine is related to increased risk for cardiovascular and other diseases in adults and elevated maternal homocysteine increases the risk for certain congenital defects, especially those that result from abnormal development of the neural crest and neural tube. Experiments with the avian embryo model have shown that elevated homocysteine perturbs neural crest / neural tube migration in vitro and in vivo. While there have been numerous studies of homocysteine-induced changes in gene expression in adult cells, there is no previous report of a homocysteine-responsive transcriptome in the embryonic neural crest. We treated neural crest cells in vitro with exogenous homocysteine in a protocol that induces significant changes in neural crest cell migration. We used microarray analysis and expression profiling to identify 65 transcripts of genes of known function that were altered by homocysteine. The largest set of effected genes (19) included those with a role in cell migration and adhesion. Other major groups were genes involved in metabolism (13); DNA / RNA interaction (11); cell proliferation / apoptosis (10); and transporter / receptor (6). Although the genes identified in this experiment were consistent with prior observations of the effect of homocysteine upon neural crest cell function, none had been identified previously as response to homocysteine in adult cells. Keywords: homocysteine ● microarray ● expression profiling ● embryo ● neural crest

2007-01-26 | GSE6868 | GEO

The effect of homocysteine on human aortic smooth muscle cells

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In the aftermath of stroke or myocardial infarction, neutrophil extracellular traps disrupt systemic immunoglobulin production

Project description:Post-injury dysfunction of humoral immunity accounts for infections and poor outcome in cardiovascular diseases. Immunoglobulin A (IgA), the most abundant mucosal antibody is produced by plasma B cells in intestinal Peyer’s patches (PP) and lamina propria. Here, we show that stroke and myocardial ischemia (MI) patients had strongly reduced IgA blood levels. This was phenocopied in experimental mouse models where decreased plasma and fecal IgA were accompanied by rapid and macroscopic shrinkage of PP caused by substantial B cell loss. Stroke/MI triggered neutrophils to release neutrophil extracellular traps (NETs). Depletion of neutrophils, NET-degradation, or blockade of NET-release inhibited PP shrinkage and loss of B cells and IgA in stroke mice. Also, stroke and MI patients had higher amounts of circulating NETs, correlating with reduced IgA levels. Strikingly, stroke patients treated with DNase-I had reduced circulating NETs and stable IgA levels. Our results unveil how tissue-injury-triggered systemic NET release disrupts physiological IgA secretion and how this can be inhibited in patients.

2024-03-17 | GSE254410 | GEO

Methyl-CpG-binding domain (MBD) sequencing of 42 primary neuroblastoma tumors

Project description:The DNA methylome of 42 primary neuroblastoma tumors is profiled by enrichment with a methyl-CpG-binding domain (MBD) and massively parallel sequencing

2015-11-19 | GSE69224 | GEO

Methyl-CpG-binding domain (MBD) sequencing of 45 primary neuroblastoma tumors

Project description:The DNA methylome of 45 primary neuroblastoma tumors is profiled by enrichment with a methyl-CpG-binding domain (MBD) and massively parallel sequencing

2015-11-19 | GSE69243 | GEO

Methyl-CpG-binding domain (MBD) sequencing of 15 primary stage 4S neuroblastoma tumors

Project description:The DNA methylome of 15 primary stage 4S neuroblastoma tumors is profiled by enrichment with a methyl-CpG-binding domain (MBD) and massively parallel sequencing

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Methyl-CpG-binding domain (MBD) sequencing of 45 primary neuroblastoma tumors

Project description:The DNA methylome of 45 primary neuroblastoma tumors is profiled by enrichment with a methyl-CpG-binding domain (MBD) and massively parallel sequencing DNA of 45 primary tumors is sheared (fragments of Â± 200 bp), followed by MBD-based (MethylCap kit of Diagenode) enrichement, library preparation and multiplexing. Both input DNA and captured DNA were sequenced paired-end on Illumina Hiseq2000

2015-11-19 | E-GEOD-69243 | biostudies-arrayexpress

Heightened Procoagulation After Post-operative Thromboprophylaxis Completion in Colorectal Cancer Patients with Metastatic Bone Disease

Project description:Platelets play a pivotal role in venous thromboembolism (VTE) and in mediating colorectal cancer (CRC) progression. Still, platelets’ role in the hypercoagulability after surgical intervention for metastatic bone diseases (MBD) is ill-defined. Here, we utilised a high-resolution imaging approach to temporally examine platelet procoagulant membrane dynamics (PMD) in four CRC patients with MBD (CRC/MBD), before and after surgical intervention, over a 6-month period. We coupled this investigation with thrombelastography, quantitative plasma shot-gun proteomics and biochemical analysis. The plasma of CRC/MBD patients was enriched in ADAM1a, ADAMTS7 and physiological ligands for platelet glycoprotein-VI (GPVI/Syk) activation. Thromboprophylaxis attenuated procoagulation from post-operative day-1 (POD1), however, all patients experienced rebound procoagulation on POD3 or POD5, which was associated with a VTE event in two patients. Plasma levels of DNA-histone complexes increased steadily after surgery and throughout the study period. Also, we increasingly sighted both homotypic and heterotypic platelet microaggregates after surgery in CRC/MBD but not healthy control participants plasma. Together, our data elucidates the cell biology of a prothrombo-inflammatory state caused by disease and vascular injury, and recalcitrant to thromboprophylaxis. New mechanistic insights into hypercoagulability in CRC/MBD patients may identify novel drug targets for effective thromboprophylaxis type and duration after orthopaedic surgery.

2023-02-23 | PXD034160 | Pride

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