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A systems biology approach identifies ANP32E and other biomarkers of glucocorticoid refractoriness in ulcerative colitis [miRNA-Seq]

ABSTRACT: A systems biology approach identifies ANP32E and other biomarkers of glucocorticoid refractoriness in ulcerative colitis [miRNA-Seq]

PROVIDER: PRJNA471862 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7178590.fastq.gz	Fastqsanger.gz
	SRR7178600.fastq.gz	Fastqsanger.gz
	SRR7178610.fastq.gz	Fastqsanger.gz
	SRR7178620.fastq.gz	Fastqsanger.gz
	SRR7178630.fastq.gz	Fastqsanger.gz

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A systems biology approach identifies ANP32E and other biomarkers of glucocorticoid refractoriness in ulcerative colitis [microarray]

Project description:BACKGROUND: Glucocorticoid (GC) refractoriness is a common and unpredictable phenomenon in ulcerative colitis (UC). Although it has been demonstrated that NFkB is involved in its mechanism of action (MoA), there are no conclusive studies on the molecular functions involved. The current study describes in depth the MoA related to GC failure, by integrating transcriptomic data from UC patients, and updated molecular data on UC and GC. METHODS: miRNA and mRNA expression from rectal biopsies of active UC patients, obtained before and on the 3rd day of GC treatment, were evaluated by sequencing and microarrays, respectively. The differential results obtained were integrated into the mathematical models generated by Systems Biology. RESULTS: This computational approach identified 64 proteins, among which 18 stand out, either by being associated to the MoA or by providing a major capacity to classify the patients according to GC response. The biological functions of these proteins have been linked with inflammation, machinery GC-induced transcription and angiogenesis. All the selected proteins but one —Acidic leucine-rich Nuclear Phosphoprotein 32 family member E (ANP32E) — had previously been related to UC and/or GC-induced biological actions. ANP32E has been linked to the exchange of H2A to H2A.z histone, which promotes CG receptor complex-activated transcription. Western blot and immunofluorescence assays confirmed the predictive results obtained by Systems Biology. CONCLUSIONS: A comprehensive MoA of GC refractoriness has been described, highlighting the key role of GC-induced transcription in this phenomenon. Several proteins have been identified as putative predictors of GC refractoriness.

2018-11-06 | GSE114527 | GEO

A systems biology approach identifies ANP32E and other biomarkers of glucocorticoid refractoriness in ulcerative colitis [miRNA-Seq]

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A systems biology approach identifies ANP32E and other biomarkers of glucocorticoid refractoriness in ulcerative colitis

Project description:A systems biology approach identifies ANP32E and other biomarkers of glucocorticoid refractoriness in ulcerative colitis

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A systems biology approach identifies ANP32E and other biomarkers of glucocorticoid refractoriness in ulcerative colitis [microarray]

Project description:A systems biology approach identifies ANP32E and other biomarkers of glucocorticoid refractoriness in ulcerative colitis [microarray]

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A systems biology approach identifies ANP32E and other biomarkers of glucocorticoid refractoriness in ulcerative colitis

Project description:This SuperSeries is composed of the SubSeries listed below.

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Systems biology approach highlights mechanistic differences between Crohn's disease and ulcerative colitis.

Project description:The molecular mechanisms of IBD have been the subject of intensive exploration. We, therefore, assembled the available information into a suite of causal biological network models, which offer comprehensive visualization of the processes underlying IBD. Scientific text was curated by using Biological Expression Language (BEL) and compiled with OpenBEL 3.0.0. Network properties were analysed by Cytoscape. Network perturbation amplitudes were computed to score the network models with transcriptomic data from public data repositories. The IBD network model suite consists of three independent models that represent signalling pathways that contribute to IBD. In the "intestinal permeability" model, programmed cell death factors were downregulated in CD and upregulated in UC. In the "inflammation" model, PPARG, IL6, and IFN-associated pathways were prominent regulatory factors in both diseases. In the "wound healing" model, factors promoting wound healing were upregulated in CD and downregulated in UC. Scoring of publicly available transcriptomic datasets onto these network models demonstrated that the IBD models capture the perturbation in each dataset accurately. The IBD network model suite can provide better mechanistic insights of the transcriptional changes in IBD and constitutes a valuable tool in personalized medicine to further understand individual drug responses in IBD.

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