2006
DOI: 10.1677/joe.1.06732
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Intestinal inflammation modulates expression of 11β-hydroxysteroid dehydrogenase in murine gut

Abstract: The effect of glucocorticoids is controlled at the pre-receptor level by the activity of 11b-hydroxysteroid dehydrogenase (11HSD). The isoform 11HSD1 is an NADP C -dependent oxidoreductase, usually reductase, that amplifies the action of glucocorticoids due to reduction of the biologically inactive 11-oxo derivatives cortisone and 11-dehydrocorticosterone to cortisol and corticosterone. The NAD C -dependent isoform (11HSD2) is an oxidase that restrains the effect of hormones due to 11b-oxidation of cortisol an… Show more

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Cited by 16 publications
(8 citation statements)
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“…The same reciprocal regulation of 11␤-HSD1 (increased) and 11␤-HSD2 (decreased) is seen in rat experimental models of colitis (96,184), with the increase in 11␤-HSD1 in colonic intraepithelial lymphocytes consistent with migration of activated lymphocytes from the inflamed colon to mesenteric lymph nodes and spleen (184,186). Mouse models of inflammatory bowel disease also show increased 11␤-HSD1 in intestinal intraepithelial lymphocytes and mesenteric lymph nodes, but 11␤-HSD2 is unchanged (724). The reciprocal regulation of 11␤-HSD1 and -2 expression in colon may be mediated by the pro-inflammatory cytokines TNF-␣ and IL-1, which decrease 11␤-HSD2 mRNA levels and enzyme activity in human SW620 colon carcinoma cells (362).…”
Section: The Gastrointestinal Tract and Inflammatory Bowel Diseasementioning
confidence: 62%
“…The same reciprocal regulation of 11␤-HSD1 (increased) and 11␤-HSD2 (decreased) is seen in rat experimental models of colitis (96,184), with the increase in 11␤-HSD1 in colonic intraepithelial lymphocytes consistent with migration of activated lymphocytes from the inflamed colon to mesenteric lymph nodes and spleen (184,186). Mouse models of inflammatory bowel disease also show increased 11␤-HSD1 in intestinal intraepithelial lymphocytes and mesenteric lymph nodes, but 11␤-HSD2 is unchanged (724). The reciprocal regulation of 11␤-HSD1 and -2 expression in colon may be mediated by the pro-inflammatory cytokines TNF-␣ and IL-1, which decrease 11␤-HSD2 mRNA levels and enzyme activity in human SW620 colon carcinoma cells (362).…”
Section: The Gastrointestinal Tract and Inflammatory Bowel Diseasementioning
confidence: 62%
“…These findings led to the hypothesis that changes in 11HSD activity induced by proinflammatory cytokines might contribute to the feedback regulation of inflammation [8,10,13]. This hypothesis is also supported by the observation that patients with inflammatory bowel diseases [14,15] and animals with experimental colitis [16][17][18][19] downregulate colonic 11HSD2 and upregulate 11HSD1. However, it is not currently known whether proinflammatory cytokines alter 11HSDs in the colon or whether inflammation modulates glucocorticoid metabolism in lymphoid organs.…”
Section: Introductionmentioning
confidence: 79%
“…Since TNBScolitis was previously found to upregulate 11HSD1 activity and mRNA expression in rat colon [15,18], we initially examined whether colitis also modulates 11HSD1 in lymphoid organs. As summarized in Fig.…”
Section: Colitis Is Associated With Upregulation Of 11-reductase Actimentioning
confidence: 99%
“…ch11HSD1 mRNA is highly expressed in the kidney, liver and intestine. Similarly, high levels of 11HSD1 transcription and protein were also found in mammalian kidney, liver and intestine [2], where 11HSD1 is not expressed in enterocytes [22] but in the subepithelial layer, in particular in immune cells [23] and fibroblasts [24]. The low level of ch11HSD1 expression in the heart and brain is probably due to the fact that this enzyme is expressed only in some cell types, such as interstitial fibroblasts of the endocardium but not in myocytes [25] and only in some brain regions such as the cerebellum and hippocampus [26,27].…”
Section: Discussionmentioning
confidence: 92%