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Intestinal adaptation and enterocyte apoptosis following small bowel resection is p53 independent

  • Cathy E. Shin
  • , Richard A. Falcone
  • , Christopher J. Kemp
  • , Christopher R. Erwin
  • , David A. Litvak
  • , B. Mark Evers
  • , Brad W. Warner

Research output: Contribution to journalArticlepeer-review

Abstract

Adaptation following small bowel resection (SBR) signals enterocyte proliferation and apoptosis. Because p53-induced p21(waf1/cip1) may be important for apoptosis in many cells, we hypothesized that these genes are required for increased enterocyte apoptosis during adaptation. Male C57BL/6 (wild-type) or p53-null mice underwent 50% proximal SBR or sham operation (bowel transection-reanastomosis). Adaptation (DNA-protein content, villus height-crypt depth, enterocyte proliferation), appearance of apoptotic bodies, and p53 and p21(waf1/cip1) protein expression were measured in the ileum after 5 days. Adaptation was equivalent after SBR in both wild-type and p53-null mice as monitored by significantly increased ileal DNA-protein content, villus height, and enterocyte proliferation. The number of crypt apoptotic bodies increased significantly after SBR evenly in both wild-type and p53-null mice. In the p53-null mice, SBR substantially induced the expression of p21(waf1/cip1) protein in villus enterocytes. The p53- independent induction of p21(waf1/cip1) may account for the similar intestinal response to SBR between wild-type and p53-null mice. Intestinal adaptation and increased enterocyte apoptosis following intestinal resection occur via a p53-independent mechanism.

Original languageEnglish
Pages (from-to)G717-G724
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Volume277
Issue number3 40-3
DOIs
StatePublished - Sep 1999

Keywords

  • Enterectomy
  • Intestinal resection
  • Mice
  • Programmed cell death
  • Short-gut syndrome

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