Here, we examined whether the formation of gap junctions could permit the exchange of specific miRs between glioblastoma and microvascular cells, and how this transfer could influence the endothelial cell function in vitro (i.e., leading to angiogenesis). We used the U87 human glioblastoma cell line and HMEC, and focused on two human mature miRs, namely miR-145-5p which is expressed in HMEC but not in U87 , and miR-5096 which is expressed in U87  but not reported in HMEC. We demonstrate an exchange of these two miRs between the two cell types through the same gap junction pathway. The effects of miR-5096, whose transfer is transiently mediated by gap junctions, starts at earliest stages of cell-cell contact and may be amplified by signal spread among HMEC. Our results reveal that glioblastoma cells modify the behavior of microvascular cells through miR transfer.