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Laboratory of Signal Transduction and the Departments of Radiation Oncology and Biostatistics, Memorial Sloan-Kettering Cancer Center, New York, New York 10021
Recent evidence suggests that microvascular endothelial apoptosis represents the primary lesion in radiation damage to the gastrointestinal (GI) tract. Rescue of endothelium by depletion of acid sphingomyelinase or i.v. treatment with basic fibroblast growth factor (FGF) prevented the lethal GI syndrome in C57Bl/6 mice. Here we show that basic FGF increased crypt survival after irradiation by 2–3 fold, with a dose modification factor at D10 of 1.15 (P < 0.01). Basic FGF inhibited initial crypt damage, assessed by crypt shrinkage at 18–24 h, but did not significantly affect the regeneration of surviving crypts at 3.5 days after irradiation. These data suggest that microvascular function regulates expression of radiation-induced crypt stem cell clonogen damage in the evolution of radiation injury to the GI mucosa.
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