Disturbances in metabolic, transport and structural genes in experimental colonic inflammation in the rat: a longitudinal genomic analysis
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AutorMartínez-Augustín, Olga; Merlos, Manel; Zarzuelo Zurita, Antonio; Suárez, María Dolores; Sánchez de Medina, Fermín
Hapten induced colitisCrohns diseaseBowel diseaseUlcerative colitisCandidate genesMicroarray dataIntestine
Martínez-Augustín, O.; et al. Disturbances in metabolic, transport and structural genes in experimental colonic inflammation in the rat: a longitudinal genomic analysis. BMC Genomics, 9: 490 (2008). [http://hdl.handle.net/10481/32815]
PatrocinadorThis study was supported by the Instituto de Investigación Carlos III (PI051651, PI051625), the Spanish Junta de Andalucía (ARM/LD 43035), the Ministry of Industry, and Fundación Genoma España.
Background: Trinitrobenzenesulphonic acid (TNBS) induced rat colitis is one of the most widely used models of inflammatory bowel disease (IBD), a condition whose aetiology and pathophysiology are incompletely understood. We have characterized this model at the genomic level using a longitudinal approach. Six control rats were compared with colitic animals at 2, 5, 7 and 14 days after TNBS administration (n = 3). The Affymetrix Rat Expression Array 230 2.0 system was used. Results: TNBS-induced colitis had a profound impact on the gene expression profile, which was maximal 5 and 7 days post-induction. Most genes were affected at more than one time point. They were related to a number of biological functions, not only inflammation/immunity but also transport, metabolism, signal transduction, tissue remodeling and angiogenesis. Gene changes generally correlated with the severity of colitis. The results were successfully validated in a subset of genes by real-time PCR. Conclusion: The TNBS model of rat colitis has been described in detail at the transcriptome level. The changes observed correlate with pathophysiological disturbances such as tissue remodelling and alterations in ion transport, which are characteristic of both this model and IBD.