Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA179142 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR611596.fastq.gz | Fastqsanger.gz | |||
| SRR611597.fastq.gz | Fastqsanger.gz | |||
| SRR611598.fastq.gz | Fastqsanger.gz | |||
| SRR611599.fastq.gz | Fastqsanger.gz | |||
| SRR611600.fastq.gz | Fastqsanger.gz |
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Project description:Objective: To define the role of epigenetics, particularly DNA methylation in adaptive vascular growth in hyperlipidemic and type 2 diabetic mouse models of hind limb ischemia Methods: Unilateral hindlimb ischemia was induced by ligating femoral artery proximal to the bifurcation of superficial and deep femoral artery. DNA was isolated from ischemic muscles collected at day 7 after ischemia induction using DNeasy Tissue kit (Qiagen). 5 µg of genomic DNA was sheared into small fragments with a mean size of 150 bp by using a Covaris⢠S2 sonicator System. Quality of the fragmentation was analyzed with Bioanalyzer. Fragmented DNA samples were used for preparation of DNA fragment libraries and sequenced on the SOLiD4 sequencing instrument on one flow cell for 50 bp reads. The sequencing reads were mapped to mus musculus genome build mm9. Data was analyzed by using Bioscope. The samples were normalized with the MEDIPS package in R/B Bioconductor. The analysis of CpG methylation was done primarily in the proximal promoter regions encompassing a region of â1kb upstream of the transcription start site (TSS) and +500 bp downstream of the TSS. Comparisons were performed between hyperlipidemic versus controls and diabetic versus controls to detect differentially methylated regions. R package Limma was used for performing the statistical testing between the groups. Results: When visualizing the whole normalized data the samples did not cluster according to the sample groups. Especially two samples from hyperlipidemic and diabetic ischemic muscles differed clearly from the rest of the samples. To detect the differentially methylated genes, stringent thresholds for p-values and fold change values were chosen to list a reasonable number of genes. Upon filtering, significant differences in the methylation patterns of the sample groups were observed. More importantly, when clustering only the filtered genes, the samples clustered clearly according to the sample groups giving evidence of condition-dependent behavior. Using a threshold of methylation fold change of >1.2 and p value <0.05, we identified 397 and 446 genes to be hypomethylated in hyperlipidemic and diabetic ischemic muscles respectively compared to controls. There were 46 genes commonly shared, but still having a unique pattern of hypomethylation in 371 and 394 genes in hyperlipidemic and diabetic ischemic muscles respectively compared to controls. Similarly, there were 371 and 394 genes hypermethylated in hyperlipidemic and diabetic ischemic respectively compared to controls. Interestingly, we found 264 genes to be commonly hypermethylated, whereas 107 and 130 genes were uniquely hypermethylated in hyperlipidemic and diabetic ischemic muscles respectively. Thus, proximal promoter methylation suggested a shared, yet distinct pattern of DNA methylation in ischemic muscles of hyperlipidemic and type 2 diabetic mice compared to controls. Out of 397 genes that were hypomethylated in hyperlipidemic ischemic muscle, 68 genes were shown to be upregulated in âproinflammatory M1 macrophagesâ as shown by recent studies. Similarly, out of the 371 hypermethylated genes 93 genes were shown to be upregulated in âanti-inflammatory and proangiogenic M2 macrophagesâ as described recently. Out of 446 hypomethylated genes in diabetic ischemic muscle, 65 genes were shown to be upregulated in âproinflammatory M1 macrophagesâ as shown recently. Similarly, out of 394 hypermethylated genes 105 genes were specifically upregulated in âanti-inflammatory and proangiogenic M2 macrophagesâ as shown recently. qRT-PCR analysis suggested an inverse relationship between proximal promoter hypermethylation and mRNA expression in a subset of M2 macrophage specific genes in hyperlipidemic and type 2 diabetic ischemic muscles compared to control ischemic muscles. Conclusions: Our results suggest a role of epigenetics particularly proximal promoter DNA methylation in macrophage polarization and their contribution to angiogenesis and tissue repair in hyperlipidemic and type 2 diabetic mouse models of hind limb ischemia. Epigenetics at the level of DNA methylation may act as a deciding factor in promoting a pro or anti-inflammatory phenotype of macrophages critical in cardiovascular diseases. Ischemic skeletal muscle DNA methylation sequencing of triplicate samples from C57BL/6J (WT) mice, hyperlipidemic mice (LDLR-/-ApoB100/100 , C57BL/6J background) and type 2 diabetic mice (IGF-II/LDLR-/-ApoB100/100 , C57BL/6J background) using SoliD4 sequencing platform
2015-12-21 | E-GEOD-42092 | biostudies-arrayexpress
Project description:Objective: To define the role of epigenetics, particularly DNA methylation in adaptive vascular growth in hyperlipidemic and type 2 diabetic mouse models of hind limb ischemia Methods: Unilateral hindlimb ischemia was induced by ligating femoral artery proximal to the bifurcation of superficial and deep femoral artery. DNA was isolated from ischemic muscles collected at day 7 after ischemia induction using DNeasy Tissue kit (Qiagen). 5 µg of genomic DNA was sheared into small fragments with a mean size of 150 bp by using a Covaris™ S2 sonicator System. Quality of the fragmentation was analyzed with Bioanalyzer. Fragmented DNA samples were used for preparation of DNA fragment libraries and sequenced on the SOLiD4 sequencing instrument on one flow cell for 50 bp reads. The sequencing reads were mapped to mus musculus genome build mm9. Data was analyzed by using Bioscope. The samples were normalized with the MEDIPS package in R/B Bioconductor. The analysis of CpG methylation was done primarily in the proximal promoter regions encompassing a region of –1kb upstream of the transcription start site (TSS) and +500 bp downstream of the TSS. Comparisons were performed between hyperlipidemic versus controls and diabetic versus controls to detect differentially methylated regions. R package Limma was used for performing the statistical testing between the groups. Results: When visualizing the whole normalized data the samples did not cluster according to the sample groups. Especially two samples from hyperlipidemic and diabetic ischemic muscles differed clearly from the rest of the samples. To detect the differentially methylated genes, stringent thresholds for p-values and fold change values were chosen to list a reasonable number of genes. Upon filtering, significant differences in the methylation patterns of the sample groups were observed. More importantly, when clustering only the filtered genes, the samples clustered clearly according to the sample groups giving evidence of condition-dependent behavior. Using a threshold of methylation fold change of >1.2 and p value <0.05, we identified 397 and 446 genes to be hypomethylated in hyperlipidemic and diabetic ischemic muscles respectively compared to controls. There were 46 genes commonly shared, but still having a unique pattern of hypomethylation in 371 and 394 genes in hyperlipidemic and diabetic ischemic muscles respectively compared to controls. Similarly, there were 371 and 394 genes hypermethylated in hyperlipidemic and diabetic ischemic respectively compared to controls. Interestingly, we found 264 genes to be commonly hypermethylated, whereas 107 and 130 genes were uniquely hypermethylated in hyperlipidemic and diabetic ischemic muscles respectively. Thus, proximal promoter methylation suggested a shared, yet distinct pattern of DNA methylation in ischemic muscles of hyperlipidemic and type 2 diabetic mice compared to controls. Out of 397 genes that were hypomethylated in hyperlipidemic ischemic muscle, 68 genes were shown to be upregulated in ‘proinflammatory M1 macrophages’ as shown by recent studies. Similarly, out of the 371 hypermethylated genes 93 genes were shown to be upregulated in ‘anti-inflammatory and proangiogenic M2 macrophages’ as described recently. Out of 446 hypomethylated genes in diabetic ischemic muscle, 65 genes were shown to be upregulated in ‘proinflammatory M1 macrophages’ as shown recently. Similarly, out of 394 hypermethylated genes 105 genes were specifically upregulated in ‘anti-inflammatory and proangiogenic M2 macrophages’ as shown recently. qRT-PCR analysis suggested an inverse relationship between proximal promoter hypermethylation and mRNA expression in a subset of M2 macrophage specific genes in hyperlipidemic and type 2 diabetic ischemic muscles compared to control ischemic muscles. Conclusions: Our results suggest a role of epigenetics particularly proximal promoter DNA methylation in macrophage polarization and their contribution to angiogenesis and tissue repair in hyperlipidemic and type 2 diabetic mouse models of hind limb ischemia. Epigenetics at the level of DNA methylation may act as a deciding factor in promoting a pro or anti-inflammatory phenotype of macrophages critical in cardiovascular diseases.
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Project description:DNA methylation marks are altered by environmental factors. We tested the hypothesis that DNA methylation is altered in skeletal muscle in response to either insulin or glucose exposure. We performed a genome-wide DNA methylation analysis in skeletal muscle from healthy men before and after insulin exposure. DNA methylation of selected genes was determined in skeletal muscle from healthy and type 2 diabetic men before and after a glucose tolerance test. Insulin reduced DNA methylation in the calcium pump ATP2A3 gene. Insulin increased DNA methylation in the gene body of death-associated protein kinase 3 (DAPK3), a gene involved in cell proliferation, apoptosis and autophagy. DAPK3 methylation was reduced in type 2 diabetic patients. Carbohydrate ingestion reduced DAPK3 DNA methylation in healthy and type 2 diabetic men, suggesting glucose may play a role. In support of this, DAPK3 DNA methylation was inversely correlated with the glucose concentration 2 hours after an oral glucose test. Insulin and glucose exposure acutely alter the DNA methylation profile of skeletal muscle, supporting recent evidence that DNA methylation constitutes a rapidly and adaptive epigenetic mark. Furthermore, insulin and glucose modulate skeletal muscle DAPK3 DNA methylation in a reciprocal manner suggesting a feedback control on the epigenome.
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2014-09-10 | E-GEOD-58280 | biostudies-arrayexpress
Project description:Monozygotic twins discordant for type 2 diabetes constitute an ideal model to study environmental contributions to type 2 diabetic traits. We aimed to examine whether global DNA methylation differences exist in major glucose metabolic tissues from twelve 53–80 year-old monozygotic discordant twin pairs. DNA methylation was measured by the Illumina HumanMethylation27 BeadChip in 22 (11 pairs) skeletal muscle and 10 (5 pairs) subcutaneous adipose tissue biopsies. No replicates were included.
2012-12-10 | E-GEOD-38291 | biostudies-arrayexpress
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