Not only angiogenesis but also inflammation participate in the pathophysiology of brain radiation necrosis

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Surgical specimens of symptomatic RN in the brain were retrospectively reviewed by histological and immunohistochemical analyses using hematoxylin and eosin (H&E) staining as well as immunohistochemical staining.The most prominent vasculature was identified as thin-walled leaky angiogenesis, i.e., telangiectasis surrounded by prominent interstitial edema.Two major cell phenotypes infiltrated the perinecrotic area: GFAP-positive reactive astrocytes and CD68/hGLUT-5-positive cells (mainly microglias). VEGF caused leaky angiogenesis followed by perilesional edema in RN. GFAP-positive cells expressing CXCL12 might attract CXCR4-expressing CD68/hGLUT5-positive cells into the perinecrotic area. These accumulated CD68/hGLUT5-positive cells expressing pro-inflammatory cytokines seemed to aggravate the RN edema. Both angiogenesis and inflammation might be caused by the regulation of HIF-1a, which is well known as a transactivator of VEGF and of the CXCL12/CXCR4 chemokine axis.