Effect of massive small bowel resection on the Bax/Bcl-w ratio and enterocyte apoptosis

Stern, Lawrence E.; Falcone, Richard A.; Kemp, Christopher J.; Stuart, Lorie A.; Erwin, Christopher R.; Warner, Brad W.

doi:10.1016/s1091-255x(00)80038-4

Cited by 36 publications

(32 citation statements)

References 40 publications

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“…We have also shown a significant increase in proapoptotic Bax gene expression and down-regulation of antiapoptotic gene Bcl-2, which may be responsible for enhanced cell apoptosis. Together with increased enterocyte proliferation, enhanced programmed cell death suggests accelerated cell turnover and is considered by many investigators as a mechanism that counterbalances the increased enterocyte mass to reach a new homeostatic set, to promote disposal of genetically aberrant stem cells, and to prevent tumorogenesis (3,4). Administration of the LEP to SBS rats reversed the increase in enterocyte apoptosis observed with SBS alone, bringing levels to that of Sham rats.…”

Section: Discussionmentioning

confidence: 99%

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Leptin Affects Intestinal Epithelial Cell Turnover in Correlation With Leptin Receptor Expression Along the Villus-Crypt Axis After Massive Small Bowel Resection in a Rat

et al. 2009

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ABSTRACT:In this study, we examine the responsiveness of intestinal epithelial cell turnover to leptin (LEP) in correlation with leptin receptor (LEPr) expression along the villus-crypt axis in a rat with short bowel syndrome (SBS). Adult rats underwent either a 75% intestinal resection or a transection. SBS-LEP rats underwent bowel resection and were treated with LEP starting from the fourth postoperative day. Parameters of intestinal adaptation, enterocyte proliferation, and enterocyte apoptosis were determined at sacrifice. RT-PCR technique was used to determine Bax and Bcl-2 gene expression in ileal mucosa. Villus tips, lateral villi, and crypts were separated using laser capture microdissection. LEPr expression for each compartment was assessed by quantitative real-time PCR (Taqman). Treatment with LEP significantly stimulated all parameters of adaptation. LEPr expression in crypts significantly increased in SBS rats (vs Sham rats) and was accompanied by a significant increase in enterocyte proliferation and decreased apoptosis after LEP administration. A significant increase in LEPr expression at the tip of the villus in SBS rats was accompanied by decreased cell apoptosis. In conclusion LEP accelerated enterocyte turnover and stimulated intestinal adaptation. The effect of LEP on enterocyte proliferation and enterocyte apoptosis correlated with receptor expression along the villus-crypt axis. (Pediatr Res 66: 648-653, 2009)

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Section: Discussionmentioning

confidence: 99%

“…Many investigators have described increased enterocyte apoptosis as a mechanism that counterbalances the increased enterocyte proliferation to reach a new homeostatic set during intestinal adaptation (4). Increased apoptosis promotes disposal of genetically aberrant stem cells and prevents tumorogenesis (3,4).…”

Section: Introductionmentioning

confidence: 99%

Leptin Affects Intestinal Epithelial Cell Turnover in Correlation With Leptin Receptor Expression Along the Villus-Crypt Axis After Massive Small Bowel Resection in a Rat

et al. 2009

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“…However, recent studies have shown that gut epithelial cells from Bcl-w-deficient mice are abnormally sensitive to g-irradiation or treatment with the cytotoxic drug 5-fluorouracil. 36 Moreover, Bcl-w levels are increased in epithelial cells adjacent to resected gut segments, 37 indicating that Bcl-w might protect against stress in this scenario. Interestingly, many human colon cancers express strikingly high levels of Bcl-w 38 ( Figure 3 and Table 1).…”

Section: Discussionmentioning

confidence: 99%

Tissue expression and subcellular localization of the pro-survival molecule Bcl-w

O’Reilly

Hausmann

et al. 2001

Cell Death Differ

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Anti-apoptotic members of the Bcl-2 family, such as Bcl-w, maintain cell viability by preventing the activation of the cell death effectors, the caspases. Gene targeting experiments in mice have demonstrated that Bcl-w is required for spermatogenesis and for survival of damaged epithelial cells in the gut. Bcl-w is, however, dispensable for physiological cell death in other tissues. Here we report on the analysis of Bcl-w protein expression using a panel of novel monoclonal antibodies. Bclw is found in a diverse range of tissues including colon, brain and testes. A survey of transformed cell lines and purified hematopoietic cells demonstrated that Bcl-w is expressed in cells of myeloid, lymphoid and epithelial origin. Subcellular fractionation and confocal laser scanning microscopy demonstrated that Bcl-w protein is associated with intracellular membranes. The implications of these results are discussed in the context of the phenotype of Bcl-w-null mice and recent data that suggest that Bcl-w may play a role in colon carcinogenesis. Cell Death and Differentiation (2001) 8, 486 ± 494.

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“…Members of the Bcl-2 family are involved in signaling pathways regulating caspase-3 activity necessary for chromatin condensation and DNA fragmentation that characterize apoptosis. The balance of pro-and antiapoptotic Bcl-2 proteins is critical for cell survival (42). We (8) and others (21) showed that an uncontrolled increase of intestinal epithelial apoptosis leads to severe NEC injury.…”

mentioning

confidence: 90%

Bifidobacterium bifidum reduces apoptosis in the intestinal epithelium in necrotizing enterocolitis

Khailová

Patrick

Arganbright

et al. 2010

American Journal of Physiology-Gastrointestinal and Liver Physi

133

100

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Necrotizing enterocolitis (NEC) is a devastating intestinal disease of neonates, and clinical studies suggest the beneficial effect of probiotics in NEC prevention. Recently, we have shown that administration of Bifidobacterium bifidum protects against NEC in a rat model. Intestinal apoptosis can be suppressed by activation of cyclooxygenase-2 (COX-2) and increased production of prostaglandin E2 (PGE2). The present study investigates the effect of B. bifidum on intestinal apoptosis in the rat NEC model and in an intestinal epithelial cell line (IEC-6), as a mechanism of protection against mucosal injury. Premature rats were divided into the following three groups: dam fed, hand fed with formula (NEC), or hand fed with formula supplemented with B. bifidum (NEC + B. bifidum ). Intestinal Toll-like receptor-2 (TLR-2), COX-2, PGE2, and apoptotic regulators were measured. The effect of B. bifidum was verified in IEC-6 cells using a model of cytokine-induced apoptosis. Administration of B. bifidum increased expression of TLR-2, COX-2, and PGE2 and significantly reduced apoptosis in the intestinal epithelium of both in vivo and in vitro models. The Bax-to-Bcl-w ratio was shifted toward cell survival, and the number of cleaved caspase-3 positive cells was markedly decreased in B. bifidum -treated rats. Experiments in IEC-6 cells showed anti-apoptotic effect of B. bifidum . Inhibition of COX-2 signaling blocked the protective effect of B. bifidum treatment in both in vivo and in vitro models. In conclusion, oral administration of B. bifidum activates TLR-2 in the intestinal epithelium. B. bifidum increases expression of COX-2, which leads to higher production of PGE2 in the ileum and protects against intestinal apoptosis associated with NEC. This study indicates the ability of B. bifidum to downregulate apoptosis in the rat NEC model and in IEC-6 cells by a COX-2-dependent matter and suggests a molecular mechanism by which this probiotic reduces mucosal injury and preserves intestinal integrity.

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Effect of massive small bowel resection on the Bax/Bcl-w ratio and enterocyte apoptosis

Cited by 36 publications

References 40 publications

Leptin Affects Intestinal Epithelial Cell Turnover in Correlation With Leptin Receptor Expression Along the Villus-Crypt Axis After Massive Small Bowel Resection in a Rat

Leptin Affects Intestinal Epithelial Cell Turnover in Correlation With Leptin Receptor Expression Along the Villus-Crypt Axis After Massive Small Bowel Resection in a Rat

Tissue expression and subcellular localization of the pro-survival molecule Bcl-w

Bifidobacterium bifidum reduces apoptosis in the intestinal epithelium in necrotizing enterocolitis

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