Nitric oxide pathway-related gene alterations in inflammatory bowel disease

Scand J Gastroenterol. 2012 Nov;47(11):1283-97. doi: 10.3109/00365521.2012.706830. Epub 2012 Aug 20.

Abstract

Objective: To reveal specific gene activation in nitric oxide (NO)-related inflammation we studied differential gene expression in inflammatory bowel disease (IBD).

Methods: Total RNA was isolated from 20 biopsies of inflamed mucosa from Crohn's disease (CD) and ulcerative colitis (UC) patients each as well as from six controls, labeled with (32)P-dCTP and hybridized to a human NO gene array. Significant genes were analyzed for functional gene interactions and heatmaps generated by hierarchical clustering. A selection of differentially expressed genes was further evaluated with immunohistochemical staining.

Results: Significant gene expression differences were found for 19 genes in CD and 23 genes in UC compared to controls, both diseases with high expression of ICAM1 and IL-8. Correlation between microarray expression and corresponding protein expression was significant (r = 0.47, p = 0.002). Clustering analysis together with functional gene interaction analysis revealed clusters of coregulation and coexpression in CD and UC: transcripts involved in angiogenesis, inflammatory response mediated by the transcription factor hypoxia-inducible factor 1, and tissue fibrosis. Also, a fourth cluster with transcripts regulated by the transcription factor Sp1 was found in UC.

Conclusions: Expression analysis in CD and UC revealed disease-specific regulation of NO-related genes, which might be involved in perpetuating inflammatory disease activity in IBD.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Aged, 80 and over
  • Case-Control Studies
  • Chi-Square Distribution
  • Cluster Analysis
  • Colitis, Ulcerative / genetics*
  • Colitis, Ulcerative / metabolism
  • Colitis, Ulcerative / pathology
  • Crohn Disease / genetics*
  • Crohn Disease / metabolism
  • Crohn Disease / pathology
  • Female
  • Fibrosis / genetics
  • Gene Expression Profiling
  • Gene Expression*
  • Humans
  • Hypoxia-Inducible Factor 1 / genetics
  • Intercellular Adhesion Molecule-1 / genetics
  • Intercellular Adhesion Molecule-1 / metabolism
  • Interleukin-1beta / genetics
  • Interleukin-1beta / metabolism
  • Interleukin-8 / genetics
  • Interleukin-8 / metabolism
  • Male
  • Matrix Metalloproteinase 1 / genetics
  • Matrix Metalloproteinase 1 / metabolism
  • Middle Aged
  • NF-kappa B / genetics
  • NF-kappa B / metabolism
  • Neovascularization, Pathologic / genetics
  • Nitric Oxide / genetics
  • Nitric Oxide / metabolism*
  • Nitric Oxide Synthase Type II / genetics
  • Nitric Oxide Synthase Type II / metabolism
  • Oligonucleotide Array Sequence Analysis
  • Signal Transduction / genetics*
  • Sp1 Transcription Factor / genetics
  • Statistics, Nonparametric
  • Young Adult

Substances

  • Hypoxia-Inducible Factor 1
  • ICAM1 protein, human
  • Interleukin-1beta
  • Interleukin-8
  • NF-kappa B
  • Sp1 Transcription Factor
  • Intercellular Adhesion Molecule-1
  • Nitric Oxide
  • Nitric Oxide Synthase Type II
  • MMP1 protein, human
  • Matrix Metalloproteinase 1