Absent STAT-1 expression perturbs adaptation and apoptosis after massive intestinal resection

Wolfgang Stehr, Nicole P. Bernal, Kathryn Q. Bernabe, Christopher R. Erwin, Brad W. Warner

Research output: Contribution to journalArticlepeer-review

5 Scopus citations


Background: We have previously established the significance of epidermal growth factor receptor (EGFR) activity and the cyclin-dependent kinase inhibitor p21waf1/cip1 (p21) for the adaptive response of the intestine to massive small bowel resection (SBR). In this study, we tested the role of the signal transducer and activator of transcription 1 (STAT-1) as this transcription factor is activated by the EGFR and known to induce p21 expression. Methods: Control (n = 40; C57/Bl6) and STAT-1-null mice (n = 40) underwent 50% proximal SBR or sham operation. After 3 days, the remnant ileum was harvested and the villus and crypt morphology was measured along with changes in rates of enterocyte proliferation and apoptosis. Results: The magnitude of resection-induced adaptation was greater in STAT-1-null animals as verified by taller villi and deeper crypts. The expected increase in enterocyte apoptosis did not occur after SBR in the background of STAT-1 deficiency. Western blotting revealed elevated expression of p21 protein in both STAT-1-null and controls after SBR. Conclusion: Increased p21 expression after SBR in the absence of STAT-1 suggests an alternate mechanism for resection-induced regulation of p21. Enhanced adaptation in STAT-1-null animals suggests that this transcription factor serves an inhibitor to the process of adaptation, perhaps via regulation of enterocyte apoptosis.

Original languageEnglish
Pages (from-to)713-718
Number of pages6
JournalJournal of Pediatric Surgery
Issue number4
StatePublished - Apr 2006


  • Adaptation
  • Apoptosis
  • Proliferation
  • STAT-1
  • Signal transducer and activator of transcription
  • Small bowel resection (SBR)
  • p21


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