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

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

Research output: Contribution to journalArticle

25 Scopus citations

Abstract

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). Apoptotic index (no. of apoptotic bodies per crypt), and bax (pro-apoptosis) and bcl-w (anti-apoptosis) protein expression was measured in the remnant ileum after 12, 24, and 72 hours. Results: Waved-2 mice with defective EGFR showed the greatest increase in apoptosis and altered the ratio of bax to bcl-w in favor of apoptosis after SBR. Conversely, EGF prevented the expected increase in apoptosis after SBR by shifting the ratio of bax to bcl-w in favor of cell survival. Conclusions: After massive small bowel resection, inhibition of the EGFR accelerates the rate of apoptosis and modifies the expression of specific bcl-2 family members to favor apoptosis. These results further support a specific mechanistic pathway for the regulation of enterocyte apoptosis after SBR via EGFR signaling.

Original languageEnglish
Pages (from-to)875-880
Number of pages6
JournalJournal of Pediatric Surgery
Volume38
Issue number6
DOIs
StatePublished - Jun 1 2003
Externally publishedYes

Keywords

  • Apoptosis
  • Bax
  • Bcl-w
  • Enterectomy
  • Epidermal growth factor receptor signaling
  • Mice
  • Small bowel resection

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