Abstract：
:Radiation is one of the most effective cancer treatments. However, gastrointestinal (GI) syndrome is a major limiting factor in abdominal and pelvic radiotherapy. The loss of crypt stem cells or villus endothelial cells has been suggested to be responsible for radiation-induced intestinal damage. We report here a critical role of the BH3-only protein p53 upregulated modulator of apoptosis (PUMA) in the radiosensitivity of intestinal epithelium and pathogenesis of GI syndrome. PUMA was induced in a p53-dependent manner and mediated radiation-induced apoptosis via the mitochondrial pathway in the intestinal mucosa. PUMA-deficient mice exhibited blocked apoptosis in the intestinal progenitor and stem cells, enhanced crypt proliferation and regeneration, and prolonged survival following lethal doses of radiation. Unexpectedly, PUMA deficiency had little effect on radiation-induced intestinal endothelial apoptosis. Suppressing PUMA expression by antisense oligonucleotides provided significant intestinal radioprotection. Therefore, PUMA-mediated apoptosis in the progenitor and stem cell compartments is crucial for radiation-induced intestinal damage.
journal_name
Cell Stem Celljournal_title
Cell stem cellauthors
Qiu W,Carson-Walter EB,Liu H,Epperly M,Greenberger JS,Zambetti GP,Zhang L,Yu Jdoi
10.1016/j.stem.2008.03.009subject
Has Abstractpub_date
2008-06-05 00:00:00pages
576-83issue
6eissn
1934-5909issn
1875-9777pii
S1934-5909(08)00122-7journal_volume
2pub_type
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