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Am J Physiol Gastrointest Liver Physiol 277: G717-G724, 1999;
0193-1857/99 $5.00
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Vol. 277, Issue 3, G717-G724, September 1999

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

Cathy E. Shin1, Richard A. Falcone Jr.1, Christopher J. Kemp1, Christopher R. Erwin1, David A. Litvak2, B. Mark Evers2, and Brad W. Warner1

1 Division of Pediatric Surgery, Children's Hospital Medical Center, Department of Surgery, University of Cincinnati College of Medicine, Cincinnati, Ohio 45229-3039; and 2 Department of Surgery, University of Texas Medical Branch, Galveston, Texas 77555-0533

Adaptation following small bowel resection (SBR) signals enterocyte proliferation and apoptosis. Because p53-induced p21waf1/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 p21waf1/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 p21waf1/cip1 protein in villus enterocytes. The p53-independent induction of p21waf1/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.

enterectomy; mice; intestinal resection; short-gut syndrome; programmed cell death


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