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Irradiation induces vessel rarefaction by differential regulation of Ang‐1, Tie‐2, Ang‐2, and VEGF in rat brain

It has been proposed that radiation‐induced brain injury is mediated by cerebrovascular rarefaction. In the present study, we investigated the molecular mechanisms of radiation‐induced vessel rarefaction in the brain. Four month old F344×BN rats received either whole brain irradiation with a single dose of 10Gy γ‐rays or sham‐irradiation, and were maintained for 4, 8, and 24 h following irradiation. A series of immunofluorescence staining revealed that whole brain irradiation significantly reduced levels of CD31‐immunoreactive cells in rat brains compared with sham‐irradiated controls. Significantly suppressed endothelial cell (EC) proliferation and increased EC apoptosis were also detected in irradiated rat brain. In addition, a significant decrease in mRNA and protein expression of angiopoietin‐1 (Ang‐1), endothelial receptor tyrosine kinase (Tie‐2), and vascular endothelial growth factor (VEGF) was observed in irradiated rat brains by real‐time RT‐PCR, ELISA, and immunofluorescence staining. In contrast, whole brain irradiation significantly up‐regulated angiopoietin‐2 (Ang‐2) expression in rat brain. These data provide the novel evidence that whole brain irradiation differentially regulates expression of Ang‐1, Tie‐2, Ang‐2 and VEGF, which may affect vessel rarefaction by decreasing EC proliferation and increasing EC apoptosis in brain. (This work was supported by NINDS R01NS056218)