Level D· Scientific groundwork from lab and animal studiesLaboratory StudyEurope PMCOpen access

Comprehensive analysis of gene expression profiles provides insight into the pathogenesis of Crohn's disease

Bo L., Fu H., Yang J.

Laboratory Study on Autoimmune Research, published in Mol Med Rep (2018) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
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This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Laboratory Study
Journal
Mol Med Rep (2018)
Reported sample size
—
Source database
Europe PMC
PMID
30015893
PMCID
PMC6102736
DOI
10.3892/mmr.2018.9267
Citations
6

Abstract (original English)

Crohn's disease (CD) is a type of inflammatory bowel disease that cannot be fully cured by medication or surgery. In the present study, the aim was to understand the underlying mechanisms of CD. Two CD microarray datasets were downloaded from The Gene Expression Omnibus database: GSE36807 (13 CD and 7 normal samples) and GSE59071 (8 CD and 11 normal samples). A series of bioinformatics analyses were conducted, including weighted gene co‑expression network analysis to identify stable modules, and analysis of differentially expressed genes (DEGs) between CD and normal samples. The common DEGs in the GSE36807 and GSE59071 datasets were screened. Subsequently, overlapping genes in the stable modules and the DEGs were selected to construct a protein‑protein interaction (PPI) network using Cytoscape software. Enrichment analysis of genes in the network was performed to explore their biological functions. A total of 10 stable modules and 927 DEGs were identified, of which 234 genes were shared in the stable modules and the DEGs. After removal of 32 uncharacterized genes, 202 genes were selected to build the PPI network. Low density lipoprotein receptor (LDLR), toll‑like receptor 2 (TLR2), lipoprotein lipase (LPL), forkhead box protein M1 (FOXM1) and neuropeptide Y (NPY) were revealed as key nodes with high degree. Pathway enrichment analysis demonstrated that LPL was enriched in the p

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
HumansCrohn DiseaseLipoprotein LipaseNeuropeptide YReceptors, LDLPeroxisome Proliferator-Activated ReceptorsComputational BiologySignal TransductionDatabases, GeneticToll-Like Receptor 2

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