Abstract
Type II 11β-hydroxysteroid dehydrogenaseendows specificity on the mineralocorticoid receptor bymetabolizing cortisol and regulates sodium absorption inrenal and colonic epithelium. Altered expression of this enzyme may be associated with impairedsodium absorption often seen in colonic mucosa ofinflammatory bowel disease. The aim of this study was toinvestigate possible abnormality of11β-hydroxysteroid dehydrogenase protein and mRNA expression ininflammatory bowel disease. In Crohn's disease, thecolonic epithelium showed comparable levels ofimmunoreactivity and mRNA expression to those ofcontrol, except for the decreased immunoreactivity insevere inflamed lesions with deep ulcer. In contrary, alack or decrease of immunoreactivity was relevant inulcerative colitis regardless of the histological degree of inflammation. The mRNA expression wasalso significantly decreased in ulcerative colitis. Thisstudy demonstrates that abnormality of epithelial cellsin ulcerative colitis includes the enzyme that regulates water and sodium absorption,which are physiologically essential.
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Takahashi, KI., Fukushima, K., Sasano, H. et al. Type II 11β-Hydroxysteroid Dehydrogenase Expression in Human Colonic Epithelial Cells of Inflammatory Bowel Disease. Dig Dis Sci 44, 2516–2522 (1999). https://doi.org/10.1023/A:1026699324927
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DOI: https://doi.org/10.1023/A:1026699324927