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Alterations of pre-mRNA splicing in human inflammatory bowel disease

Robert Häsler1, Martin Kerick, Nancy Mah

  • 1Institute of Clinical Molecular Biology, Christian-Albrechts-University, Schittenhelmstrasse 12, 24105 Kiel, Germany. r.haesler@mucosa.de

European Journal of Cell Biology
|February 18, 2011
PubMed

Insights

Alternative pre-mRNA splicing plays a key role in chronic inflammation, particularly in inflammatory bowel diseases (IBD). This study identified numerous differentially regulated splicing factors and intron retention events in IBD patients, highlighting their pathogenic potential.

Area of Science:

  • Molecular Biology
  • Genetics
  • Immunology

Background:

  • Alternative pre-mRNA splicing generates proteome diversity.
  • Aberrant splicing is linked to diseases, but its role in chronic inflammation is unclear.
  • Inflammatory bowel diseases (IBD) are chronic inflammatory conditions.

Purpose of the Study:

  • To investigate the role of alternative splicing in inflammatory bowel diseases (IBD).
  • To identify differentially regulated splicing factors and intron retention events in IBD.
  • To analyze subtype-specific splicing changes in Crohn's disease and ulcerative colitis.

Main Methods:

  • Systematic screening of 149 splicing factors and 145 intron retention events in IBD mucosal tissue.
  • Differential expression analysis at the transcript level.
  • Validation of seven splicing factors and three intron retention events using real-time PCR in a cohort of 165 patients and 30 controls.

Main Results:

  • Identified 47 splicing factors and 33 intron retention events differentially regulated in IBD.
  • Observed shared and significant subtype-specific splicing changes between Crohn's disease and ulcerative colitis.
  • Quantified expression levels of key splicing factors and intron retention events in inflammatory conditions.

Conclusions:

  • Regulated splicing factors potentially impact subsequent intron retention in chronic inflammation pathogenesis.
  • Alternative splicing alterations are implicated in the pathophysiology of IBD.
  • This study provides insights into the molecular mechanisms underlying chronic inflammatory diseases.

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