Epidermal growth factor receptor signaling regulates goblet cell production after small bowel resection.

Background/purpose: Intestinal adaptation is a compensatory response to massive small bowel loss in which there are increased numbers of absorptive enterocytes. However, the generation of secretory epithelial cell subtypes in this process has not been investigated. The purpose of this study was to examine the adaptive changes of several small intestinal cell lineage changes in response to massive small bowel resection (SBR).

Bax deficiency rescues resection-induced enterocyte apoptosis in mice with perturbed EGF receptor function.

Background: Adaptation after massive smallbowel resection (SBR) is associated with increased cell turnover, increased rates of enterocyte proliferation, and apoptosis. Epidermal growth factor receptor (EGFR) inhibition attenuates adaptation and increases apoptosis. Intestinal levels of bax appear to correlate with EGFR signaling.

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).

A serum factor(s) after small bowel resection induces intestinal epithelial cell proliferation: effects of timing, site, and extent of resection.

Background/purpose: After small bowel resection (SBR), serum induces proliferation in rat intestinal epithelial cells (RIEC-6). This study was designed to elucidate the effects of postoperative time interval, site, and magnitude of SBR on RIEC-6 proliferation.

Methods: Serum was collected from rats at various times after a 75% mid-SBR or sham operation and added to RIEC-6 cells and growth determined over 5 days.

Reoperative venous access.

The maintenance of long-term venous access is critical to the livelihood of children in a variety of clinical situations, especially those who are dependent on parenteral nutrition. Whereas the traditional routes of either peripheral or central venous access are initially adequate, most of these sites eventually succumb to the pitfalls associated with long-term venous access. This review provides a comprehensive and multidisciplinary approach to the management of reoperative venous access with regard to preoperative planning and imaging and specific techniques in interventional radiology and surgery.

Enterocyte apoptosis after enterectomy in mice is activated independent of the extrinsic death receptor pathway.

Intestinal adaptation following small bowel resection (SBR) is associated with greater rates of enterocyte apoptosis by unknown mechanism(s). Because postresection adaptation is associated with increased translocation of luminal bacteria, we sought to characterize the role for the extrinsic, death receptor pathway for the activation of enterocyte apoptosis after massive SBR. We first performed SBR or sham operations in mice, and the temporal expression of caspases 8, 9, and 3, death receptors tumor necrosis factor receptor-1 (TNFR1) and Fas and corresponding ligands (TNF and Fas ligand) was determined in the remnant intestine at various postoperative time points.

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.

A serum factor after intestinal resection stimulates epidermal growth factor receptor signaling and proliferation in intestinal epithelial cells.

Background: In vivo, intestinal adaptation after massive small bowel resection (SBR) requires a functional epidermal growth factor (EGF) receptor (EGFR). In vitro studies have shown that serum from mice after SBR induces rat intestinal epithelial cells to proliferate. This study tested the hypothesis that the proliferative response to SBR serum is mediated by EGFR signaling.