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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE278779 | GEO | 2025/10/01

REPOSITORIES: GEO

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Project description:Signaling pathways controlling vasculogenesis and angiogenesis are still poorly understood. Zebrafish Ets1-related protein (Etsrp) which encodes an ETS domain transcription factor, evolutionary related to the mammalian ER71 protein subfamily, has been identified as a major regulator of vasculogenesis and myelopoiesis and functions at the hemangioblast stage affecting the formation of both lineages. In the absence of Etsrp, angioblasts do not migrate or differentiate while overexpression of Etsrp results in the expansion of vascular endothelial and myeloid lineages. To identify genes functioning downstream of Etsrp we performed microarray analysis of etsrp-overexpressing embryos. Etsrp RNA injected embryos and control uninjected embryos were frozen at the tailbud stage and analyzed for expression of more than 30,000 genes using Nimblegen expression arrays. Approximately 300 genes showed greater than two-fold induction in etsrp-overexpressing embryos. Scl, crl, egfl7, aqp8, fli1a, fli1b, lmo2, cdh5 were among the previously known hemangioblast or vasculature-specific genes which were strongly upregulated in Etsrp-overexpressing embryos. We isolated and characterized a number of genes that were novel or previously unassociated with the zebrafish vasculature formation. Eight of them which include angiotensin II type 2 receptor (agtr2), src homology 2 domain containing E (she), similar to mannose receptor C1 (mrc1), endothelial cell-specific adhesion molecule (esam), cdc42 guanine nucleotide exchange factor 9 (arhgef9), yes-related kinase (yrk), zinc finger protein, multitype 2b (zfpm2b/fog2b) and stabilin 2 (stab2) were specifically expressed in vascular endothelial cells during early embryonic development while keratin18 expression was localized to the myeloid cells among others. Identification of novel vasculature and myeloid-specific genes that are regulated by Etsrp will be important for dissecting molecular mechanisms that regulate vasculogenesis / angiogenesis and myelopoiesis.

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

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