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

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).

Smooth muscle overexpression of IGF-I induces a novel adaptive response to small bowel resection.

Prior studies of intestinal adaptation after massive small bowel resection (SBR) have focused on growth factors and their effects on amplification of the gut mucosa. Because adaptive changes have also been described in intestinal smooth muscle, we sought to determine the effect of targeted smooth muscle growth factor overexpression on resection-induced intestinal adaptation. Male transgenic mice with smooth muscle cell overexpression of insulin-like growth factor I (IGF-I) by virtue of an alpha-smooth muscle actin promoter were obtained.

Characterization of small bowel resection and intestinal adaptation in germ-free rats.

Background: After massive small bowel resection (SBR), the remnant bowel adapts by increasing enterocyte proliferation and apoptosis. The purpose of this study was to investigate the relevance of luminal bacteria on postresection intestinal cell turnover.

Methods: Male germ-free (GF) and normally colonized control rats underwent either a 75% mid-SBR or sham operation.

EGF receptor signaling affects bcl-2 family gene expression and apoptosis after massive small bowel resection.

Background: After massive small bowel resection (SBR), enterocyte apoptosis is elevated and inversely correlates with epidermal growth factor receptor (EGFR) signaling. The purpose of the current study was to determine whether EGFR manipulation affects the expression of specific bcl-2 family members.

Methods: A 50% proximal SBR or sham operation was performed in 3 groups of mice control, after exogenous EGF, or mutant mice with defective EGFR signaling (waved-2).

Localization of postresection EGF receptor expression using laser capture microdissection.

Background/purpose: Epidermal growth factor (EGF) and its receptor (EGFR) are key components in the genesis of adaptation after small bowel resection (SBR). Within intestinal homogenates, EGFR expression is increased after SBR; however, the exact cells responsible for altered EGFR expression are unknown. In this study, laser capture microdissection (LCM) microscopy was used to elucidate the specific cellular compartment(s) responsible for postresection changes in EGFR expression.