The glial cells missing 1 triggers gliosis and vasculogenesis after neonatal brain injury [ChIP-Seq]

The glial cells missing (gcm) protein in Drosophila plays a crucial role in the cell fate switch in the nervous system and in induction of glial cell differentiation. However, the functions of the mammalian homologue Gcm1 in normal neural development and pathological conditions remain elusive. Here, we report that Gcm1 was upregulated in Nestin+ cells immediately after neonatal brain injury, 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 actions of VEGF-A and VEGF-C. Lack of Gcm1-mediated vasculogenesis could be a major cause of the dysplasia in placental labyrinths found in Gcm1–/– embryos, leading to embryonic lethality. Our data suggest that Gcm1 triggers both gliosis and vasculogenesis after brain injury and could be a target for therapeutic intervention. ChIP-seq for HA was performed for mouse neuroblastoma Neuro2a cells.