Permeability Change of the Endothelial Monolayer Co-cultured with Glioma or Glioblastoma Cell Lines by Dexamethasone

Abstract

Even though many hypotheses have been advanced from the anatomical and functional analysis of in vivo and in vitro models of brain tumors, it is still not yet possible to explain the mechanism of peritumoral edema. Dexamethasone administration has been shown to dramatically decrease peritumoral edema, especially in patients with malignant brain tumor. We evaluated permeability changes of the endothelial monolayer co-cultured with or without glioma and glioblastoma cell lines by dexamethasone administration. All groups showed reduced permeability after dexamethasone administration: 73.6% in the endothelial monolayer culture, 83.8% in the endothelial monolayer co-cultured with C6 glioma cell line, 81.8% in the coculture with H683 astrocytoma cell line, 69.3% in the coculture with 373 MG glioblastoma cell line, and 53.0% in the coculture with 87 MG glioblastoma cell line. These results suggested that dexamethasone inhibited not only the production of some soluble factor which was secreted from the co-cultured cells to the media, but also influenced endothelial cells thus explaining the pathogenetic mechanism of peritumoral edema in malignant brain tumors.