Bax is required for increased enterocyte apoptosis after massive small bowel resection

Stern, Lawrence E.; Huang, Frederick S.; Kemp, Christopher J.; Falcone, Richard A.; Erwin, Christopher R.; Warner, Brad W.

doi:10.1067/msy.2000.107370

Cited by 53 publications

(51 citation statements)

References 19 publications

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“…Cell loss in the small intestine is mainly regulated by the programmed cell death (23). Several studies have recently shown that EC apoptosis is increased in the frame of intestinal adaptation after P-SBR, and emphasized that bax is the major protein that drives increased EC apoptosis after SBR (11,24,25). On the other hand, others have also reported an increased expression of Fas, another potent inducer of apoptosis over the death receptor pathway after P-SBR (13).…”

Section: Discussionmentioning

confidence: 99%

Influence of the site of small bowel resection on intestinal epithelial cell apoptosis

et al. 2005

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Section: Discussionmentioning

confidence: 99%

Influence of the site of small bowel resection on intestinal epithelial cell apoptosis

et al. 2005

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“…Following small bowel resection, there is increased crypt cell apoptosis in the adapting mouse intestine (13,37), presumably as a protective mechanism to eliminate damaged stem cells following injury. This increase was accompanied by increased expression of Fas/Fas ligand (37) and was blocked in Bax-null mice (34,37), implicating the extrinsic death receptor and Bax/Bcl2 pathways in this response. Others have shown that Fas/Fas ligand apoptotic pathways are regulated by Hh, e.g., inhibition of Hh signaling in basal cell carcinoma cell lines leads to increased apoptosis and increased Fas expression (1).…”

Section: Discussionmentioning

confidence: 99%

Increased apoptosis and accelerated epithelial migration following inhibition of hedgehog signaling in adaptive small bowel postresection

Tang¹,

Swietlicki²,

Jiang³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Following SBR, increased expression of the proapoptotic protein Bax has been recorded in enterocytes, which correlates with augmented rates of apoptosis (4,13,27,36,38). Furthermore, using Bax-null mice, we have established that Bax expression is required for resection-induced apoptosis (22,37).…”

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confidence: 98%

p38 MAPK regulates Bax activity and apoptosis in enterocytes at baseline and after intestinal resection

Wakeman

Guo

Santos

et al. 2012

American Journal of Physiology-Gastrointestinal and Liver Physi

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Increased apoptosis in crypt enterocytes is a key feature of intestinal adaptation following massive small bowel resection (SBR). Expression of the proapoptotic factor Bax has been shown to be required for resection-induced apoptosis. It has also been demonstrated that p38-α MAPK (p38) is necessary for Bax activation and apoptosis in vitro. The present studies were designed to test the hypothesis that p38 is a key regulator of Bax activation during adaptation after SBR in vivo. Enterocyte expression of p38 was deleted by tamoxifen administration to activate villin-Cre in adult mice with a floxed Mapk14 (p38-α) gene. Proximal 50% SBR or sham operations were performed on wild-type (WT) and p38 intestinal knockout (p38-IKO) mice under isoflurane anesthesia. Mice were killed 3 or 7 days after operation, and adaptation was analyzed by measuring intestinal morphology, proliferation, and apoptosis. Bax activity was quantified by immunoprecipitation, followed by Western blotting. After SBR, p38-IKO mice had deeper crypts, longer villi, and accelerated proliferation compared with WT controls. Rates of crypt apoptosis were significantly lower in p38-IKO mice, both at baseline and after SBR. Levels of activated Bax were twofold higher in WT mice after SBR relative to sham. In contrast, activated Bax levels were reduced by 67% in mice after p38 MAPK deletion. Deleted p38 expression within the intestinal epithelium leads to enhanced adaptation and reduced levels of enterocyte apoptosis after massive intestinal resection. p38-regulated Bax activation appears to be an important mechanism underlying resection-induced apoptosis.

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Bax is required for increased enterocyte apoptosis after massive small bowel resection

Cited by 53 publications

References 19 publications

Influence of the site of small bowel resection on intestinal epithelial cell apoptosis

Influence of the site of small bowel resection on intestinal epithelial cell apoptosis

Increased apoptosis and accelerated epithelial migration following inhibition of hedgehog signaling in adaptive small bowel postresection

p38 MAPK regulates Bax activity and apoptosis in enterocytes at baseline and after intestinal resection

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