Influence of the site of small bowel resection on intestinal epithelial cell apoptosis

Abstract

Background-Massive small bowel resection (SBR) results in a significant increase in intestinal epithelial cell (EC) proliferation as well as apoptosis. Because the site of SBR (proximal (P) vs. distal (D)) affects the degree of intestinal adaptation, we hypothesized that different rates of EC apoptosis would also be found between P-SBR and D-SBR models.

Epidermal growth factor receptor signaling modulates apoptosis via p38α MAPK-dependent activation of Bax in intestinal epithelial cells

“…This observation has been confirmed by other investigators (12,(22)(23)(24). Given the highly dynamic nature of the intestinal mucosa, elevated rates of apoptosis probably serve to counter the increased rates of enterocyte proliferation, thus preserving a critical homeostatic balance.…”

p38 MAPK regulates Bax activity and apoptosis in enterocytes at baseline and after intestinal resection

“…Coupled with increased Bax expression (4,13,27,36,38) this finding suggests that the activity of endogenous Bax is also a contributor toward the elevated rates of enterocyte apoptosis observed after SBR. Furthermore, we provide evidence supporting our hypothesis that Bax activation is mediated by p38 MAPK in vivo.…”

“…Based on these findings, we have, therefore, focused on elucidating how the intrinsic pathway mediates gut apoptosis during adaptation. Following SBR, increased expression of the proapoptotic protein Bax has been recorded in enterocytes, which correlates with augmented rates of apoptosis (4,13,27,36,38). Furthermore, using Bax-null mice, we have established that Bax expression is required for resection-induced apoptosis (22,37).…”

Inhibition of ACE activity contributes to the intestinal structural compensation in a massive intestinal resection rat model

“…We found that both ANGII receptors subtypes AT1R and AT2R expressed on intestinal mucosa surface of the rats after small bowel transection or resection. It showed that the minimum immunoreactivity for angiotensin II receptor subtype 1 (AT1R) appeared in the SBS group rats Pediatr Surg Int (2012) 28:533-541 539 intestinal mucosa at 7 days in an SBS mouse model [14]. ACE-I treatment to rats after SBR revealed higher intestinal mucosa structural adaptation.…”

“…Intestinal adaptation after SBR in rodents is structurally characterized by an increase in ECs proliferation and apoptosis rates [14,15]. The precise mechanisms for these changes have not been clearly understood.…”