Project description:Gene expression of X-irradiated primary murine astrocytes Roggan MD, Kronenberg J, Wollert E, Hoffmann S, Nisar H, Konda B, Diegeler S, Liemersdorf C and Hellweg CE (2023) Unraveling astrocyte behavior in the space brain: Radiation response of primary astrocytes. Front. Public Health 11:1063250.
Project description:Cultured primary human astrocytes were maintained in HA media (SciCell) treated with 0 Gy or 10 Gy radiation to identify changes to gene sets after irradiation.
Project description:Cdca7l acts as a male-specific oncogene in astrocytoma and glioblastoma, and can transform primary astrocyte growth in soft agar. We stably overexpressed Cdca7l in mouse primary astrocytes and compared gene expression to primary astrocytes expressing empty vector control in male and female cell to identify gene expression differences between male and female cells and between Cdca7l-overexpressing and normal primary astrocytes.
Project description:Primary cultures of astrocytes from rat optic nerve heads were treated with EGFR ligand, EGF. Two cell lines from two different rat donors were used. The sister cell cultures were set as control and EGF treated groups. Keywords: rat optic nerve head astrocytes
Project description:Affymetrix Mouse Genome 430 2.0 GeneChip microarrays were used to analyze murine neocortical and cerbellar astrocytes generated from postnatal (PN) day 1 wild-type (ICR) pups. Experiment Overall Design: Three samples each of murine neocortical and cerebellar astrocytes were analyzed.
Project description:Introduction: Glioma stem cells isolated from human glioblastomas are resistant to radiation and cytotoxic chemotherapy and may drive tumor recurrence. Treatment efficacy may depend on the presence of glioma stem cells, expression of DNA repair enzymes such as methylguanine methyltransferase (MGMT), or transcriptome subtype. Methods: To model genetic alterations in the core signaling pathways of human glioblastoma, we induced conditional Rb knockout, Kras activation, and Pten deletion mutations in cortical murine astrocytes. Serial neurosphere culture, multi-lineage differentiation, and orthotopic transplantation were used to assess whether these mutations induced de-differentiation of cortical astrocytes into glioma stem cells. Efficacy of radiation and temozolomide was examined in vitro and in an allograft model in vivo. The effects of radiation on transcriptome subtype was examined by expression profiling. Results: G1/S-defective, Rb knockout astrocytes gained unlimited self-renewal and multi-lineage differentiation capacity, in both the presence and absence of Kras and Pten mutations. Only triple mutant astrocytes formed serially-transplantable glioblastoma allografts. Triple mutant astrocytes and allografts were sensitive to radiation, but expressed Mgmt and were resistant to temozolomide. Radiation induced a shift in transcriptome subtype of glioblastoma allografts from proneural to mesenchymal. Conclusion: A defined set of core signaling pathway mutations induces de-differentiation of cortical murine astrocytes into glioma stem cells. This non-germline genetically engineered mouse model mimics human proneural glioblastoma on histopathological, molecular, and treatment response levels. It may be useful in dissecting the genetic and cellular mechanisms of treatment resistance and developing more effective therapies.
