Intercellular adhesion molecule-1 (ICAM-1) upregulation in human brain tumors as an expression of increased blood-brain barrier permeability.

The distribution of intercellular adhesion molecule (ICAM-1) binding sites was studied in the microvasculature of several types of human brain tumor biopsies (angioma, glioblastoma multiforme and meningioma). Immunoelectron microscopy was performed with the application of immuno-HRP or -gold probes using a pre-embedding technique. Ultrastructural analysis demonstrated a pronounced ICAM-1 upregulation on the luminal EC and/or perivascular surfaces. Reaction product for ICAM-1 was observed associated with some but not all blood vessels of the tumors examined. The strongest reaction product was noted associated with the angioma cases with lesser expression observed on the glioblastoma multiforme and meningioma cases. The reaction product using immuno-HRP probe was observed most pronounced on the luminal endothelial cell surface and also within vesiculo-tubular structures. Concentrated immunosignals with gold label were often expressed on EC microvilli. These data suggest that several types of brain tumors are actively involved in the process of upregulating ICAM-1, presumably for tumor cell adhesion and trafficking, the process of angiogenesis or both. We suggest that the ICAM-1-positive vesiculo-tubular structures reflect specialized, targeted regions on the ECs for tumor cell adhesion and eventual trans-BBB passage. Further, our studies also provide evidence that adhesion molecules may be a useful tool for the study of blood-brain barrier injury.