Epigenome analysis of fetal and adult liver samples
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE61278 | GEO | 2014/09/18
SECONDARY ACCESSION(S): PRJNA260642
REPOSITORIES: GEO
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Project description:Genome wide DNA methylation analysis of 96 adult and 14 fetal liver samples The study includes 110 individuals, 14 fetal and 96 adult samples, no replicates. Liver samples from 14 fetuses were obtained at gestational week 8-12. Adult liver samples were collected from 52 organ donors who had met accidental death and 44 liver samples from patients undergoing liver resection due to malignant tumors, most commonly from patients with metastatic colon cancers. Liver biopsies from these patients were collected from 'healthy' tissue that showed no visible pathological changes compared to the adjacent tumor.
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Project description:Genome wide expression analysis of 92 adult and 14 fetal liver samples
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Project description:DNA methylation is an important epigenetic control mechanism that has been shown to be associated with gene silencing through the course of development, maturation and aging. However, only limited data are available regarding the relationship between methylation and gene expression in human development. We analyzed the methylomes and transcriptomes of three human fetal liver samples (gestational age 20-22 weeks) and three adult human liver samples. Genes whose expression differed between fetal and adult numbered 7,673. Adult overexpression was associated with metabolic pathways and, in particular, cytochrome P450 enzymes while fetal overexpression reflected enrichment for DNA replication and repair. Analysis for DNA methylation using the Illumina Infinium 450K HumanMethylation BeadChip showed that 42% of the quality filtered 426,154 methylation sites differed significantly between adult and fetal tissue (q≤0.05). Differences were small; 69% of the significant sites differed in their mean methylation beta value by ≤0.2. There was a trend among all sites toward higher methylation in the adult samples with the most frequent difference in beta being 0.1. Characterization of the relationship between methylation and expression revealed a clear difference between fetus and adult. Methylation of genes overexpressed in fetal liver showed the same pattern as seen for genes that were similarly expressed in fetal and adult liver. In contrast, adult overexpressed genes showed fetal hypermethylation that differed from the similarly expressed genes. An examination of gene region-specific methylation showed that sites proximal to the transcription start site or within the first exon with a significant fetal-adult difference in beta (>0.2) showed an inverse relationship with gene expression. Nearly half of the CpGs in human liver show a significant difference in methylation comparing fetal and adult samples. Sites proximal to the transcription start site or within the first exon that show a transition from hypermethylation in the fetus to hypomethylation or intermediate methylation in the adult are associated with inverse changes in gene expression. In contrast, increases in methylation going from fetal to adult are not associated with fetal-to-adult decreased expression. These findings indicate fundamentally different roles for and/or regulation of DNA methylation in human fetal and adult liver.
2015-12-29 | GSE69852 | GEO
Project description:DNA methylation is an important epigenetic control mechanism that has been shown to be associated with gene silencing through the course of development, maturation and aging. However, only limited data are available regarding the relationship between methylation and gene expression in human development. We analyzed the methylomes and transcriptomes of three human fetal liver samples (gestational age 20-22 weeks) and three adult human liver samples. Genes whose expression differed between fetal and adult numbered 7,673. Adult overexpression was associated with metabolic pathways and, in particular, cytochrome P450 enzymes, while fetal overexpression reflected enrichment for DNA replication and repair. Analysis for DNA methylation using the Illumina Infinium 450K HumanMethylation BeadChip showed that 42% of the quality filtered 426,154 methylation sites differed significantly between adult and fetal tissue (q≤0.05). Differences were small; 69% of the significant sites differed in their mean methylation beta value by ≤0.2. There was a trend among all sites toward higher methylation in the adult samples with the most frequent difference in beta being 0.1. Characterization of the relationship between methylation and expression revealed a clear difference between fetus and adult. Methylation of genes overexpressed in fetal liver showed the same pattern as seen for genes that were similarly expressed in fetal and adult liver. In contrast, adult overexpressed genes showed fetal hypermethylation that differed from the similarly expressed genes. An examination of gene region-specific methylation showed that sites proximal to the transcription start site or within the first exon with a significant fetal-adult difference in beta (>0.2) showed an inverse relationship with gene expression. Nearly half of the CpGs in human liver show a significant difference in methylation comparing fetal and adult samples. Sites proximal to the transcription start site or within the first exon that show a transition from hypermethylation in the fetus to hypomethylation or intermediate methylation in the adult are associated with inverse changes in gene expression. In contrast, increases in methylation going from fetal to adult are not associated with fetal-to-adult decreased expression. These findings indicate fundamentally different roles for and/or regulation of DNA methylation in human fetal and adult liver.
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Project description:Genome wide expression analysis of 92 adult and 14 fetal liver samples The study includes 106 individuals, 14 fetal and 92 adult samples, no replicates. Liver samples from 14 fetuses were obtained at gestational week 8-12. Adult liver samples were collected from 50 organ donors who had met accidental death and 42 liver samples from patients undergoing liver resection due to malignant tumors, most commonly from patients with metastatic colon cancers. Liver biopsies from these patients were collected from 'healthy' tissue that showed no visible pathological changes compared to the adjacent tumor.
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Project description:In human F8 deficiency leads to hemophilia A and is largely synthesized and secreted by the sinusoidal endothelial cells of the liver (LSECs). However, the specificity and characteristics of these cells is not well known. In this study, we performed genome wide expression and CpG methylation profiling of fetal and adult human LSECs together with other fetal endothelial cells, from lung (micro-vascular and arterial), and heart (micro-vascular). Our results reveal plenty of expression and methylation markers distinguishing LSECs at both fetal and adult stages. Differential gene expression of fetal LSECs in comparison to other fetal endothelial cells pointed to several differential regulated pathways and functions in fetal LSECs. We used targeted bisulfite re-sequencing to confirm selected top differentially methylated regions. We further designed an assay where we used the selected methylation markers to test the degree of similarity of in house iPSs generated vascular endothelial cells to fetal and adult LSECs; a higher similarity was found to the fetal than to adult LSECs. Our molecular profiling study provides a guide to test the effectiveness of production of in vitro differentiated LSECs that could be used in cellular therapies. In-silico analysis to identify molecular signature of liver sinusoidal endothelial cells in comparison to other endohtelial cells
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Project description:In human F8 deficiency leads to hemophilia A and is largely synthesized and secreted by the sinusoidal endothelial cells of the liver (LSECs). However, the specificity and characteristics of these cells is not well known. In this study, we performed genome wide expression and CpG methylation profiling of fetal and adult human LSECs together with other fetal endothelial cells, from lung (micro-vascular and arterial), and heart (micro-vascular). Our results reveal plenty of expression and methylation markers distinguishing LSECs at both fetal and adult stages. Differential gene expression of fetal LSECs in comparison to other fetal endothelial cells pointed to several differential regulated pathways and functions in fetal LSECs. We used targeted bisulfite re-sequencing to confirm selected top differentially methylated regions. We further designed an assay where we used the selected methylation markers to test the degree of similarity of in house iPSs generated vascular endothelial cells to fetal and adult LSECs; a higher similarity was found to the fetal than to adult LSECs. Our molecular profiling study provides a guide to test the effectiveness of production of in vitro differentiated LSECs that could be used in cellular therapies. In-silico analysis to identify molecular signature of liver sinusoidal endothelial cells in comparison to other endohtelial cells
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Project description:In human F8 deficiency leads to hemophilia A and is largely synthesized and secreted by the sinusoidal endothelial cells of the liver (LSECs). However, the specificity and characteristics of these cells is not well known. In this study, we performed genome wide expression and CpG methylation profiling of fetal and adult human LSECs together with other fetal endothelial cells, from lung (micro-vascular and arterial), and heart (micro-vascular). Our results reveal plenty of expression and methylation markers distinguishing LSECs at both fetal and adult stages. Differential gene expression of fetal LSECs in comparison to other fetal endothelial cells pointed to several differential regulated pathways and functions in fetal LSECs. We used targeted bisulfite re-sequencing to confirm selected top differentially methylated regions. We further designed an assay where we used the selected methylation markers to test the degree of similarity of in house iPSs generated vascular endothelial cells to fetal and adult LSECs; a higher similarity was found to the fetal than to adult LSECs. Our molecular profiling study provides a guide to test the effectiveness of production of in vitro differentiated LSECs that could be used in cellular therapies. In-silico analysis to identify molecular signature of liver sinusoidal endothelial cells in comparison to other endohtelial cells
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Project description:In human F8 deficiency leads to hemophilia A and is largely synthesized and secreted by the sinusoidal endothelial cells of the liver (LSECs). However, the specificity and characteristics of these cells is not well known. In this study, we performed genome wide expression and CpG methylation profiling of fetal and adult human LSECs together with other fetal endothelial cells, from lung (micro-vascular and arterial), and heart (micro-vascular). Our results reveal plenty of expression and methylation markers distinguishing LSECs at both fetal and adult stages. Differential gene expression of fetal LSECs in comparison to other fetal endothelial cells pointed to several differential regulated pathways and functions in fetal LSECs. We used targeted bisulfite re-sequencing to confirm selected top differentially methylated regions. We further designed an assay where we used the selected methylation markers to test the degree of similarity of in house iPSs generated vascular endothelial cells to fetal and adult LSECs; a higher similarity was found to the fetal than to adult LSECs. Our molecular profiling study provides a guide to test the effectiveness of production of in vitro differentiated LSECs that could be used in cellular therapies. In-silico analysis to identify molecular signature of liver sinusoidal endothelial cells in comparison to other endohtelial cells
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