Preventing enterocyte apoptosis after massive small bowel resection does not enhance adaptation of the intestinal mucosa

Russell J. Juno, Andrew W. Knott, Sherri A. Profitt, Marcus D. Jarboe, Yufang Zhang, Christopher R. Erwin, Brad W. Warner

Research output: Contribution to journalArticle

20 Scopus citations

Abstract

Background After massive small bowel resection (SBR), increased rates of enterocyte apoptosis are observed in the remnant bowel via a mechanism requiring bax gene expression. This study tested the hypothesis that adaptive mucosal growth could be enhanced by the novel strategy of preventing postresection enterocyte apoptosis. Methods Male bax-null and corresponding wild-type (WT) mice underwent a 50% proximal SBR or sham operation (bowel transaction with reanastomosis alone). Mice were killed after a full adaptation interval of 1 month. Adaptation was measured in the remnant ileum as alterations in villus height, crypt depth, and wet weight. Rates of enterocyte proliferation were derived by immunostaining of crypt enterocytes for Ki-67 and apoptosis by the presence of apoptosis bodies. Results The expected increase in enterocyte apoptosis after SBR occurred in the WT mice but was unchanged in the bax-null mice. Despite the prevention of postresection apoptosis in the bax-null mice, all parameters of adaptation and proliferation increased equally after SBR in both groups of mice. Conclusions Bax deficiency prevents the increase in enterocyte apoptosis that occurs after massive SBR throughout the entire adaptation period. Attenuation of postresection enterocyte apoptosis does not augment mucosal adaptation to massive intestinal loss.

Original languageEnglish
Pages (from-to)907-911
Number of pages5
JournalJournal of Pediatric Surgery
Volume39
Issue number6
DOIs
StatePublished - Jun 1 2004
Externally publishedYes

Keywords

  • Short gut syndrome
  • adaptation enterocyte
  • apoptosis
  • enterectomy
  • knockout mice
  • small bowel resection

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