Rat IUGR islet transcriptome sequencing at 2 time points
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA407958 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6051200.fastq.gz | Fastqsanger.gz | |||
| SRR6051201.fastq.gz | Fastqsanger.gz | |||
| SRR6051192.fastq.gz | Fastqsanger.gz | |||
| SRR6051202.fastq.gz | Fastqsanger.gz | |||
| SRR6051193.fastq.gz | Fastqsanger.gz |
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Project description:Intrauterine growth restriction (IUGR) increases the risk of developing type 2 diabetes during adulthood. At day 18 of gestation, we used bilatual uterine artery ligation (BUAL) to restrict nutrient supply to developing rat fetuses to produce IUGR pups. At 2 and 10 weeks of age pancreatic islets were isolated and total RNA extracted using Trizol. Samples with RNA integrity numbers greater than 7 were used to generate libraries
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Project description:Intrauterine growth restriction (IUGR) increases the risk of developing type 2 diabetes in adulthood. A rat model of IUGR induced by bilateral uterine artery ligation at day 18 of gestation, which reduces the blood supply and critical substrates to the fetus, was used to assess the alterations of genome-wide histone modifications in IUGR islets. At 2 and 10 weeks of age, pancreatic islets were isolated and chromatins were extracted for ChIP-Seq study. Chromatin state of H3K4me3, H3K27me3, and H3K27Ac modifications was compared in the study.
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Project description:Intrauterine growth restriction (IUGR) increases the risk of developing type 2 diabetes in adulthood. A rat model of IUGR induced by bilateral uterine artery ligation at day 18 of gestation, which reduces the blood supply and critical substrates to the fetus, was used to assess the alterations of genome-wide DNA methylation in IUGR islets. At 2 weeks of age, pancreatic islets were isolated and genomic DNA were extracted for TruSeq-HELP tagging assay. Cytosine methylation was compared in the study.
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Project description:Intrauterine growth restriction (IUGR) increases susceptibility to age-related diseases including type 2 diabetes (T2DM), and is associated with permanent and progressive changes in gene expression and epigenetic regulation. We studied cytosine methylation throughout the genome in pancreatic islets from a rat model of uteroplacental insufficiency, providing a novel and detailed assessment of the genomic distribution and locus-specific patterns of DNA methylation in normal islets as well as the changes that occur as a consequence of IUGR. Utilizing a high throughput approach to study DNA methylation at almost 1 million unique sites throughout the genome, we found ~1,400 changes in methylation (IUGR compared to control) with an estimated false discovery rate of 4.2%. These epigenetic differences were observed in IUGR male rats at 7 weeks of age, preceding the development of diabetes in this model. Therefore, these epigenetic differences represent candidates for mediating the pathogenesis of metabolic disease that occurs later in life in these animals. Moreover, many of the changes we identify are located near genes that regulate processes known to be abnormal in IUGR islets, such as vascularization, β-cell proliferation, insulin secretion, and cell death. Consistent changes in mRNA expression were identified at some of the epigenetically-dysregulated genes including Fgfr1, Gch1, Pcsk5, and Vgf. Globally, epigenetic dysregulation occurred preferentially at conserved intergenic sequences, which are candidate cis-regulatory elements driving differential expression of nearby genes. These results provide insights into the complex developmental consequences of IUGR, and suggest that changes in DNA methylation could mediate a constellation of changes in both gene expression and pancreatic islet development and function, with relevance to T2DM.
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Project description:We performed RNA microarray in a low protein diet (LPD) model of IUGR at three key time points of alveolarization process. IUGR and control rat pups had been studied for each time point considered: on postnatal day 4 (P4) before beginning of the alveolarization process, on P10, peak of alveolarization process and on P21 at the end of it.
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