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Bax is required for increased enterocyte apoptosis after massive small bowel resection
1Division of Pediatric Surgery, Children's Hospital Medical Center, Department of Surgery, University of Cincinnati College of Medicine, OH 45229-3039, USA.
Surgery
|August 3, 2000
Summary
Massive small bowel resection (SBR) increases apoptosis, but the bax gene is not required for this response. Bax is necessary for increased apoptosis after SBR, but its absence does not affect short-term intestinal adaptation.
Area of Science:
- Gastroenterology
- Cell Biology
- Surgical Research
Background:
- Massive small bowel resection (SBR) elevates enterocyte proliferation and apoptosis.
- Increased proapoptotic bax mRNA and protein expression, along with an 18-kd bax cleavage product, are observed within 12 hours of SBR.
- Previous research indicates a potential role for bax in post-SBR apoptosis.
Purpose of the Study:
- To investigate whether the bax gene is essential for the increase in enterocyte apoptosis following SBR.
- To determine the role of bax in the adaptive changes in the small intestine after resection.
Main Methods:
- Male bax-null and control mice underwent 50% proximal small bowel resection (SBR) or sham operation.
- Ileum was harvested after 3 days to assess wet weight, apoptotic index, proliferation index, villus height, and crypt depth.
Main Results:
- Adaptive increases in ileal wet weight, crypt depth, and proliferation were observed in both control and bax-null mice post-SBR.
- SBR significantly increased apoptosis in control mice but not in bax-null mice.
- The absence of bax did not affect short-term adaptive changes in the ileum.
Conclusions:
- Bax is indispensable for the post-SBR surge in enterocyte apoptosis.
- Bax deficiency does not impede short-term intestinal adaptation following SBR.
- Enterocyte proliferation and apoptosis appear to be independently regulated during intestinal adaptation.