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

• Published in: Journal of pediatric surgery Vol. 39; no. 6; pp. 907 - 911
• Main Authors: Juno, Russell J., Knott, Andrew W., Profitt, Sherri A., Jarboe, Marcus D., Zhang, Yufang, Erwin, Christopher R., Warner, Brad W.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.06.2004
• Subjects: adaptation enterocyte; Adaptation, Physiological; Animals; Apoptosis; bcl-2-Associated X Protein; Cell Division; enterectomy; Enterocytes - pathology; Ileum - pathology; Ileum - surgery; knockout mice; Male; Mice; Mice, Knockout; Proto-Oncogene Proteins c-bcl-2 - deficiency; Random Allocation; Regeneration; Short Bowel Syndrome - prevention & control; Short gut syndrome; Single-Blind Method; small bowel resection; apoptosis; Short gut syndrome; knockout mice; small bowel resection; adaptation enterocyte; enterectomy
• ISSN: 0022-3468; 1531-5037
• DOI: 10.1016/j.jpedsurg.2004.02.007

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. 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. 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. 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.