RNA- and ChIP-seq analysis of cytokine treated islets
Transcriptomics Dataset
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| Accession | GSE73289 |
| Title | RNA- and ChIP-seq analysis of cytokine treated islets |
| Description | Purpose: In the early phases of T1D development exposure of -cells to IFN, IL-1, and TNF is thought to induce -cell dysfunction and the expression of chemokines and cytokines. These changes are mediated in part by post-translational histone modifications within cis-regulatory regions. The purpose of this study was to determine if prevention of these epigenetic changes can alter cytokine induced gene expression changes. Methods: Pancreatic islets were isolated from both male and female CD1 mice by collagenase digestion and were picked by hand. Hand-picked islets were cultured for four days with 1.6ng/ml IFN, 0.25ng/ml IL-1 and 0.16ng/ml TNF (cytokine) or were left untreated (nocytokine). For RNA-seq islets were collected and processed for NGS using the Illumina TruSeq library prep kit. Chromatin immunoprecipitation (ChIP) was performed using 3g of anti-H3K4me1 (Abcam) with islets from at least 10 adult ICR mice (8-10 weeks old) exposed to 1.6ng/ml IFN, 0.25ng/ml Il-1 and 0.16ng/ml TNF for four days. DNA from 4 separate ChIP experiments was pooled for library construction and sequencing using the Illumina platform. Results: Comparison of gene expression levels between untreated and cytokine-treated islets resulted in the identification of 205 genes that showed an IFN, Il-1, and TNF-induced chromatin state change (from repressed or inactive to H3K4me1 enriched, i.e. the de novo regions), or increased H3K4me1 enrichment, that were associated with genes with up-regulated expression in response to IFN, Il-1, and TNF, and 111 genes with reduced H3K4me1 and down-regulated expression in response to IFN, Il-1, and TNF. Conclusions: Our study confirms that exposure of islets to pro-inflammatory cytokines induces the expression of chemokines and that these changes are the result of a switch from an inactive to an active chromatin state. Further we show that disruption of the trithorax group complex inhibits the upregulation of pro-inflammatory gene expression. |
| Landing Page | https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE73289 |
| Repository | Gene Expression Omnibus |
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