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.