DNA microarray technology reveals similar gene expression patterns in rats with vitamin a deficiency and chemically...

Previous studies suggest that vitamin A deficiency may induce or intensify inflammatory changes in the rat gastrointestinal system. The present study was designed to compare the expression profiles of rat models of vitamin A deficiency and induced colitis. cDNA-microarray technology was used to determine the genes involved in the inflammatory processes in the two models. mRNA was extracted from colons of rats that were vitamin A deficient, vitamin A supplemented (control), or had 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis, reverse-transcribed into fluorescence-labeled cDNA and hybridized onto microarrays containing a duplicate set of 1152 cDNAs, derived mainly from the colon carcinoma cell line Caco-2. Differential gene expression was detected in vitamin A deficiency and in TNBS-induced colitis vs. control. beta-Actin, translation initiation factor A4 and translation elongation factor 1, ornithine decarboxylase (ODC) and keratin 19 were markedly down-regulated, whereas spermidine/spermine N1-acetyltransferase (SSAT) and polyubiquitin (UbC) were up-regulated in both vitamin A-deficient rats and those with TNBS-induced colitis. The strong association between the differential gene expression in the two animal models, compared with the control, suggests that deficiency of vitamin A causes inflammatory changes in the rat colon that are similar to processes occurring in colitis. Further investigation is required to elucidate the importance of each of the regulated genes to the pathology of colitis and vitamin A inadequacy.