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

27 Scopus citations


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
Issue number3 40-3
StatePublished - Sep 1999


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

ASJC Scopus subject areas

  • Physiology
  • Hepatology
  • Gastroenterology
  • Physiology (medical)


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