期刊
FREE RADICAL RESEARCH
卷 41, 期 1, 页码 8-14出版社
TAYLOR & FRANCIS LTD
DOI: 10.1080/10715760600913150
关键词
Radiation fibrosis; TGF-beta; VEGF; ROS; SOD-mimetic; macrophages
资金
- NCI NIH HHS [R01 CA098452-01] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA098452] Funding Source: NIH RePORTER
Normal tissue injury poses a major limitation to the success of radiation therapy (RT) in the treatment of solid tumors. We propose that radiation-induced lung injury is a result of chronic oxidative stress propagated by hypoxia-induced macrophage activation and cytokine production. Therefore, the objective of our study was two-fold. First, in vivo studies were conducted to support our hypothesis suggesting radiation injury is characterized by chronic hypoxia associated with increased macrophage infiltration/activation and pro-fibrogenic/angiogenic cytokine production. Second, we investigated the proposed mechanism of radiation injury in vitro. We demonstrate that hypoxia (0.5% O-2) elicits macrophages to produce higher levels of O-2(center dot-), TGF-beta, and VEGF than normoxia. Our hypothesis that O-2(center dot-) is contributing to increased macrophage cytokine production was supported by a significant reduction in TGF-beta and VEGF when redox signaling was minimized using a small molecular weight metalloporphyrin antioxidant, MnTE-2-PyP5+.
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