Epigenetic alterations are associated with gastric emptying disturbances in Diabetes Mellitus
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ABSTRACT:
PROVIDER: PRJNA596193 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10720100_1.fastq.gz | Fastqsanger.gz | |||
| SRR10720100_2.fastq.gz | Fastqsanger.gz | |||
| SRR10720101_1.fastq.gz | Fastqsanger.gz | |||
| SRR10720101_2.fastq.gz | Fastqsanger.gz | |||
| SRR10720102_1.fastq.gz | Fastqsanger.gz |
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Project description:Introduction. Epigenetic modifications have been implicated to mediate several complications of diabetes mellitus (DM), especially nephropathy and retinopathy. Our aims were to ascertain if epigenetic alterations in whole blood discriminate among DM patients with normal, delayed and rapid gastric emptying (GE). Methods. Using ChIP-seq (Chromatin immunoprecipitation combined with next generation sequencing) assays, we compared the genome-wide enrichment of three histone modifications (ie, H3K4me3, H3K9ac and H3K27ac) in buffy coats from 20 DM patients with normal (n=6), delayed (n=8), or rapid (n=6) GE. Results. Between DM patients with delayed versus normal GE, there were 108 and 54 genes that were differentially-bound (FDR < 0.05) with H3K27ac and H3K9ac; 100 genes were differentially bound with H3K9ac in patients with rapid versus normal GE. The differentially bound genes with H3K27ac were functionally linked to the type 2 immune response, particularly Th2 cell activation and function (eg, CCR3, CRLF2, CXCR4, IL5RA, and IL1RL1) and glucose homeostasis (FBP-1, PDE4A, CMKLR1). For H3K9ac, the differentially occupied genes were related to T cell development and function (eg, ICOS and CCR3) and innate immunity (RELB, CD300LB, CLEC2D). Compared to normal, rapid GE had differential H3K9ac peaks at the promoter site of diverse immunity-related genes (eg, TNFRSF25 and CXCR4) and genes related to insulin resistance and glucose metabolism. The motif analysis disclosed enrichment of binding sites for several transcription factors relevant to the pathogenesis and complications of DM. Conclusions. GE disturbances in DM are associated with epigenetic alterations that may serve as biomarkers and provide clues to the pathogenesis
2021-12-26 | GSE142178 | GEO
Project description:IntroductionEpigenetic modifications have been implicated to mediate several complications of diabetes mellitus (DM), especially nephropathy and retinopathy. Our aim was to ascertain whether epigenetic alterations in whole blood discriminate among patients with DM with normal, delayed, and rapid gastric emptying (GE).MethodsUsing the ChIP-seq (chromatin immunoprecipitation combined with next-generation sequencing) assays, we compared the genome-wide enrichment of 3 histone modifications (i.e., H3K4me3, H3K9ac, and H3K27ac) in buffy coats from 20 diabetic patients with gastrointestinal symptoms and normal (n = 6), delayed (n = 8), or rapid (n = 6) GE.ResultsBetween patients with DM with delayed vs normal GE, there were 108 and 54 genes that were differentially bound (false discovery rate < 0.05) with H3K27ac and H3K9ac, respectively; 100 genes were differentially bound with H3K9ac in patients with rapid vs normal GE. The differentially bound genes with H3K27ac were functionally linked to the type 2 immune response, particularly Th2 cell activation and function (e.g., CCR3, CRLF2, CXCR4, IL5RA, and IL1RL1) and glucose homeostasis (FBP-1, PDE4A, and CMKLR1). For H3K9ac, the differentially occupied genes were related to T-cell development and function (e.g., ICOS and CCR3) and innate immunity (RELB, CD300LB, and CLEC2D). Compared with normal GE, rapid GE had differential H3K9ac peaks at the promoter site of diverse immunity-related genes (e.g., TNFRSF25 and CXCR4) and genes related to insulin resistance and glucose metabolism. Motif analysis disclosed enrichment of binding sites for transcription factors relevant to the pathogenesis and complications of DM.DiscussionGE disturbances in DM are associated with epigenetic alterations that pertain to dysimmunity, glucose metabolism, and other complications of DM.
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Project description:Systemic epigenetic alterations are associated with gastric emptying disturbances in Non-Ulcer Dyspepsia
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Project description:Background. The mechanisms by which environmental risk factors (eg, stress) predispose to symptoms and gastric emptying (GE) disturbances in non-ulcer dyspepsia (NUD) is unknown. Our aims were to compare the circulating leukocytes’ epigenome between NUD patients with normal versus delayed and normal versus rapid GE. Methods. In 24 NUD patients, we evaluated gastrointestinal symptoms, GE (scintigraphy) and 3 promoter/enhancer-associated histone modifications (H3K4me3, H3K9ac, and H3K27ac) by chromatin immunoprecipitation-sequencing in buffy coats, then compared the genome-wide binding of histone marks between patients with normal versus delayed and normal versus rapid GE. Key results. GE was normal (9 patients), delayed (6 patients), or rapid (9 patients). Compared to normal GE, there was differential binding of H3K4me3, which marks active promoters, at 100 genes in delayed and 233 genes in rapid GE (FDR < 0.05). Delayed GE was associated with increased H3K4me3 binding at several genes that regulate T cell functions (eg, CD247, IL2RA, CD69, CD96, ICOS, ITK, and GRAP2); conversely, binding was reduced at genes that regulate neuronal synapses (ie, SYT6, SYT12, CDH2, CDH11, EFNB3, CAMK2B, and SHISA6) and neuronal nitric oxide synthase (NOS1). In rapid GE, genes related to opioid signaling (OPRD1, MAPK4, CAMK2B, and PDE1C), neuronal development, and synaptic functions bound less H3K4me3. No or few genes were differentially enriched with H3K9ac and H3K27ac. Conclusions. H3K4me3 discriminates among patients with normal, rapid, and delayed GE. Delayed GE is associated with alterations that suggest increased T-cell functions. Rapid GE is associated with changes suggesting reduced opioid signaling.
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Project description:Proteomics is a powerful approach to study the molecular mechanisms of cancer. In this study, we aim to characterize the proteomic profile of gastric cancer (GC) in patients with diabetes mellitus (DM) type 2. Forty GC tissue samples including 19 cases from diabetic patients and 21 cases from individuals without diabetes (control group) were selected for the proteomics analysis. Gastric tissues were processed following the single-pot, solid-phase-enhanced sample preparation approach—SP3 and enzymatic digestion with trypsin. The resulting peptides were analyzed by LC-MS Liquid Chromatography—Mass Spectrometry (LC-MS). The comparison of protein expression levels between GC samples from diabetic and non-diabetic patients was performed by label-free quantification (LFQ). A total of 6599 protein groups were identified in the 40 samples. Thirty-seven proteins were differentially expressed among the two groups, with 16 upregulated and 21 downregulated in the diabetic cohort. Statistical overresentation tests were considered for different annotation sets including the Gene Ontology(GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), Reactome, and Disease functional databases. Upregulated proteins in the GC samples from diabetic patients were particularly enriched in respiratory electron transport and alcohol metabolic biological processes, while downregulated proteins were associated with epithelial cancers, intestinal diseases, and cell–cell junction cellular components. Taken together, these results support the data already obtained by previous studies that associate diabetes with metabolic disorders and diabetes-associated diseases, such as Alzheimer’s and Parkinson’s, and also provide valuable insights into seven GC-associated protein targets, claudin-3, polymeric immunoglobulin receptor protein, cadherin-17, villin-1, transglutaminase-2, desmoglein-2, and mucin-13, which warrant further investigation.
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