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Enterocyte apoptosis after enterectomy in mice is activated independent of the extrinsic death receptor pathway.
Am J Physiol Gastrointest Liver Physiol. 2003 Aug; 285(2):G404-13.AJ

Abstract

Intestinal adaptation following small bowel resection (SBR) is associated with greater rates of enterocyte apoptosis by unknown mechanism(s). Because postresection adaptation is associated with increased translocation of luminal bacteria, we sought to characterize the role for the extrinsic, death receptor pathway for the activation of enterocyte apoptosis after massive SBR. We first performed SBR or sham operations in mice, and the temporal expression of caspases 8, 9, and 3, death receptors tumor necrosis factor receptor-1 (TNFR1) and Fas and corresponding ligands (TNF and Fas ligand) was determined in the remnant intestine at various postoperative time points. Ileal TNFR1 and Fas expression were then measured after SBR in the setting of increased (waved-2 mice) or decreased (exogenous EGF administration) apoptosis. Finally, intestinal adaptation and apoptosis were recorded in the remnant ileum after SBR in TNFR1-null and Fas-null mice. The expression of death receptor family proteins and caspases demonstrated only modest changes after SBR and did not correlate with the histological appearance of apoptosis. In the setting of accelerated apoptosis, TNFR1 and Fas expression were paradoxically decreased. Apoptotic and adaptive responses were preserved in both TNFR1-null and Fas-null mice. These results suggest that the mechanism for increased enterocyte apoptosis following massive SBR does not appear to involve the extrinsic, death receptor-mediated pathway.

Authors+Show Affiliations

Knott AW
Division of Pediatric Surgery, Cincinnati Children's Hospital Medical Center, OH 45229-3039, USA.
O'Brien DP
No affiliation info available
Juno RJ
No affiliation info available
Zhang Y
No affiliation info available
Williams JL
No affiliation info available
Erwin CR
No affiliation info available
Warner BW
No affiliation info available

MeSH

AnimalsAntigens, CDApoptosisCaspase 3Caspase 8Caspase 9CaspasesEnterocytesEpidermal Growth FactorFas Ligand ProteinIntestine, SmallKineticsMaleMembrane GlycoproteinsMiceMice, Inbred C3HMice, Inbred C57BLMice, KnockoutReceptors, Tumor Necrosis FactorReceptors, Tumor Necrosis Factor, Type ITumor Necrosis Factor-alphafas Receptor

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

12724132

Citation

Knott, Andrew W., et al. "Enterocyte Apoptosis After Enterectomy in Mice Is Activated Independent of the Extrinsic Death Receptor Pathway." American Journal of Physiology. Gastrointestinal and Liver Physiology, vol. 285, no. 2, 2003, pp. G404-13.
Knott AW, O'Brien DP, Juno RJ, et al. Enterocyte apoptosis after enterectomy in mice is activated independent of the extrinsic death receptor pathway. Am J Physiol Gastrointest Liver Physiol. 2003;285(2):G404-13.
Knott, A. W., O'Brien, D. P., Juno, R. J., Zhang, Y., Williams, J. L., Erwin, C. R., & Warner, B. W. (2003). Enterocyte apoptosis after enterectomy in mice is activated independent of the extrinsic death receptor pathway. American Journal of Physiology. Gastrointestinal and Liver Physiology, 285(2), G404-13.
Knott AW, et al. Enterocyte Apoptosis After Enterectomy in Mice Is Activated Independent of the Extrinsic Death Receptor Pathway. Am J Physiol Gastrointest Liver Physiol. 2003;285(2):G404-13. PubMed PMID: 12724132.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Enterocyte apoptosis after enterectomy in mice is activated independent of the extrinsic death receptor pathway. AU - Knott,Andrew W, AU - O'Brien,David P, AU - Juno,Russell J, AU - Zhang,Yufang, AU - Williams,Jodi L, AU - Erwin,Christopher R, AU - Warner,Brad W, Y1 - 2003/04/30/ PY - 2003/5/2/pubmed PY - 2003/8/30/medline PY - 2003/5/2/entrez SP - G404 EP - 13 JF - American journal of physiology. Gastrointestinal and liver physiology JO - Am J Physiol Gastrointest Liver Physiol VL - 285 IS - 2 N2 - Intestinal adaptation following small bowel resection (SBR) is associated with greater rates of enterocyte apoptosis by unknown mechanism(s). Because postresection adaptation is associated with increased translocation of luminal bacteria, we sought to characterize the role for the extrinsic, death receptor pathway for the activation of enterocyte apoptosis after massive SBR. We first performed SBR or sham operations in mice, and the temporal expression of caspases 8, 9, and 3, death receptors tumor necrosis factor receptor-1 (TNFR1) and Fas and corresponding ligands (TNF and Fas ligand) was determined in the remnant intestine at various postoperative time points. Ileal TNFR1 and Fas expression were then measured after SBR in the setting of increased (waved-2 mice) or decreased (exogenous EGF administration) apoptosis. Finally, intestinal adaptation and apoptosis were recorded in the remnant ileum after SBR in TNFR1-null and Fas-null mice. The expression of death receptor family proteins and caspases demonstrated only modest changes after SBR and did not correlate with the histological appearance of apoptosis. In the setting of accelerated apoptosis, TNFR1 and Fas expression were paradoxically decreased. Apoptotic and adaptive responses were preserved in both TNFR1-null and Fas-null mice. These results suggest that the mechanism for increased enterocyte apoptosis following massive SBR does not appear to involve the extrinsic, death receptor-mediated pathway. SN - 0193-1857 UR - https://www.unboundmedicine.com/medline/citation/12724132/Enterocyte_apoptosis_after_enterectomy_in_mice_is_activated_independent_of_the_extrinsic_death_receptor_pathway_ DB - PRIME DP - Unbound Medicine ER -