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Absent STAT-1 expression perturbs adaptation and apoptosis after massive intestinal resection
Wolfgang Stehr1, Nicole P Bernal, Kathryn Q Bernabe
1Division of Pediatric General and Thoracic Surgery, Department of Surgery, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH 45229-3039, USA.
Journal of Pediatric Surgery
|March 29, 2006
Summary
Signal transducer and activator of transcription 1 (STAT-1) deficiency enhances intestinal adaptation after small bowel resection (SBR). STAT-1-null mice show greater villus height and crypt depth, suggesting STAT-1 inhibits adaptation.
Area of Science:
- Gastroenterology
- Molecular Biology
- Cellular Biology
Background:
- Epidermal growth factor receptor (EGFR) activity and p21waf1/cip1 (p21) are crucial for intestinal adaptation post-small bowel resection (SBR).
- Signal transducer and activator of transcription 1 (STAT-1) is activated by EGFR and induces p21 expression.
Purpose of the Study:
- To investigate the role of STAT-1 in the adaptive response of the intestine following SBR.
- To determine if STAT-1 influences p21 expression and enterocyte apoptosis after SBR.
Main Methods:
- Control and STAT-1-null mice underwent 50% proximal SBR or sham operation.
- Ileum was harvested 3 days post-surgery to assess villus and crypt morphology, enterocyte proliferation, and apoptosis.
Main Results:
- STAT-1-null mice exhibited enhanced intestinal adaptation with significantly taller villi and deeper crypts compared to controls.
- Enterocyte apoptosis did not increase after SBR in STAT-1-null mice.
- Elevated p21 protein expression was observed in both STAT-1-null and control mice post-SBR.
Conclusions:
- Absence of STAT-1 leads to increased p21 expression, indicating an alternative pathway for p21 regulation after SBR.
- STAT-1 appears to inhibit intestinal adaptation post-SBR, potentially by regulating enterocyte apoptosis.
