2010
DOI: 10.1002/ibd.21031
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Epithelial vanin-1 controls inflammation-driven carcinogenesis in the colitis-associated colon cancer model

Abstract: These results emphasize the importance of the intestinal epithelium in the control of mucosal inflammation acting as a cofactor in carcinogenesis. This might lead to novel anti-inflammatory strategies useful in cancer therapy.

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Cited by 51 publications
(42 citation statements)
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“…Based upon these observations, vanin-1-deficeint mice were administered cysteamine or cystamine, an oxidized form of cysteamine, to determine if cysteamine alone can recover the inflammatory response. Results show that the vanin-1-deficeint mice supplemented with cysteamine had a similar inflammatory response to control wildtype mice (12,17,18,21,23,24). This suggests that cysteamine is a key molecule that induces inflammatory response and is a possible route for medical intervention.…”
Section: Cysteamine -A Key Player In Inflammation and Host Defensementioning
confidence: 78%
See 1 more Smart Citation
“…Based upon these observations, vanin-1-deficeint mice were administered cysteamine or cystamine, an oxidized form of cysteamine, to determine if cysteamine alone can recover the inflammatory response. Results show that the vanin-1-deficeint mice supplemented with cysteamine had a similar inflammatory response to control wildtype mice (12,17,18,21,23,24). This suggests that cysteamine is a key molecule that induces inflammatory response and is a possible route for medical intervention.…”
Section: Cysteamine -A Key Player In Inflammation and Host Defensementioning
confidence: 78%
“…On the other hand, cysteamine has a protective feature against malaria infection, although the precise mechanisms remain to be elucidated (hatched arrows pointing upward). Unable to metabolize pantetheine in liver and kidney, very low tissue cysteamine levels (11) Increase in the level of reduced form of glutathione in tissues (12,17) g-glutamylcysteine synthetase activity (12) Delayed death caused by administration of lethal dose of paraquat (12) g-irradiation (12) 2,4,6-trinitrobenezene sulfonic acid (18) Schistosoma mansoni infection (17) Suppression of intestinal inflammation caused by administration of indomethacin and Schistosoma mansoni infection (17) unusual bone marrow stromal cells and chondrogenic transdifferentiation and calcification of aortic smooth muscle cells derived from ank/ank mice (20) incidence of colitis-associated colon cancer (24) granuloma formation in liver and spleen after the infection with Coxiella burnetii (21) the incidence of diabetes in NOD mice (23) Decrease in selenium-independent glutathione peroxidase activity and the GSTA3 protein level (22) Failure to induce inflammatory mediators including cytokines in response to stress (12,17,18,21,23,24) Induction of peroxisome proliferator activator receptor-g (18) activity and the GSTA3 protein (22). In humans, GSH/ GSSG levels are inversely correlated to VNN1 gene expression levels in chronic idiopathic thrombocytopenic purpura patients.…”
Section: Cysteamine -A Key Player In Inflammation and Host Defensementioning
confidence: 99%
“…For example, VNN1-deficient mice are resistant to intestinal inflammation, oxidative stress, and experimental colitis (15,16). VNN1 also plays a critical role in malaria susceptibility, psoriasis, carcinogenesis, and cardiovascular disease (29)(30)(31)(32). Importantly, the vnn1 gene is one of the major targets of PPARa in the mouse liver, which strongly implies that VNN1 is involved in the regulation of energy metabolism (18).…”
Section: Discussionmentioning
confidence: 99%
“…Similarly to the previously investigated in vivo models (9 -13), in Sf-1 TR/Vnn1 Ϫ/Ϫ mice the effect of Vnn1 inactivation could be reversed by administration of cysteamine, the product of the enzymatic activity of Vanin-1. Conversely, at variance with the colitis-induced colon cancer model (13), the tumorigenic process induced by Sf-1 overexpression in the adrenal is not associated with inflammatory cells infiltration and cytokine production (data not shown). These findings suggest that intracellular redox systems have an important role to control tumorigenesis in the adrenal cortex, as indicated by high expression of Vnn1 in the dysplastic cell population ( Figure 2F).…”
Section: Discussionmentioning
confidence: 52%
“…Vnn1 Ϫ/Ϫ mice then have a higher intracellular content of glutathione in their tissues, which correlates with a lower reactive oxygen species concentration and higher resistance to oxidative stress (9) and reduced sensitivity to both acute and chronic intestinal inflammation (10,11). Vnn1 inactivation also significantly reduces tumor formation in the colitis-associated colon cancer model (13) and decreases oxidative stress, proliferation, and migration in vascular smooth muscle cells (22).…”
Section: Discussionmentioning
confidence: 95%