Glial cells missing 1 triggers gliosis and vasculogenesis in the neonatal brain injury

glial cells missing (gcm) in Drosophila plays a crucial role in the fate switch in nervous system and induces glial differentiation. However, function of a mammalian homologue, Gcm1, in the normal neural development and in pathological conditions remains elusive. Here, we report that Gcm1 was upregulated in Nestin+ cells immediately after neonatal brain injury was made, followed by accumulation of GFAP+ and Olig2+ cells in the penumbra region. In addition, Gcm1 strongly induced vasculogenesis in the injury lesion as well as in the developing brain via the action of VEGFA and VEGFC. Lack of Gcm1-mediated vasculogenesis could be one of major causes for dysplasia of placental labyrinths found in Gcm1–/– embryos, which leads to embryonic lethality. Our data suggest that Gcm1 triggers both gliosis and vasculogenesis after brain injury and could be a target for therapeutic intervention. Overall design: The transcriptome profiles of the GFP-positive tissues from Gcm1 overexpression and control embryonic mouse brains (E16.5) were generated using the Illumina HiSeq platforms. The number of replicates for both Gcm1 overexpression and control samples is five.