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Sojka, C.

Publications and source records attributed to Sojka, C..

3 recordsLinked to original sources

Region-specific human brain organoids reveal synaptic and cell state drivers of glioblastoma invasion

Glioblastoma (GBM) is a highly heterogenous and malignant brain tumor, in part because it disrupts normal brain circuits to fuel its own growth and invasion. Thus, there is a need to identify the molecular features of invasive GBM cells and their regulators in the neural microenvironment. To address this in a fully human model, we engrafted patient-derived GBM cells (total n=15 independent samples) from three sources-- fresh neurosurgical resections, cell lines, and whole GBM organoids--into human induced pluripotent stem cell-derived organoids patterned to forebrain, midbrain, and spinal cord identities. GBM cells from all sources infiltrated brain organoids within 2 days post-engraftment, reaching maximal invasion by day 14. Across organoids of distinct spatial and maturational milieu, GBM cells showed a consistent reduction in astrocyte-like states and an enrichment in neuron/glia progenitor-like (NPC-like) states. These NPC-like GBM cells expressed neuronal and synaptic machinery, and tumors enriched in this transcriptomic state prior to engraftment achieved greater organoid coverage, suggesting enhanced infiltration and synaptic integration of this GBM cell type. Although GBM cell states converged across organoid types after engraftment, infiltration was greater in the forebrain than spinal cord. This is likely reflective of synaptic input from deep-layer TBR1 excitatory neurons in the forebrain, as demonstrated by a combination of rabies-based monosynaptic tracing and single-cell transcriptomics. In contrast, inhibitory neurons were the predominant synaptic partners of GBM in the spinal cord. Together, this fully human model of the neural-GBM connectome reveals how neuron-like GBM states and regionally distinct synaptic inputs cooperatively shape tumor invasion.

neuroscience↗

Temporal regulation of human reactive astrocytes reveals their capacity for antigen presentation

Astrocytes adapt to injury and disease by entering a reactive state defined by transcriptomic, morphological, and functional changes. Using a combination of human cortical organoids (hCOs) and primary fetal brain tissue, we investigated the plasticity of human astrocyte reactivity. We observed robust inflammatory transcriptomic and chromatin signatures following cytokine exposure, which varied with duration. To assess reversibility, we withdrew cytokines after acute or chronic exposure. In both cases, astrocytes returned to a quiescent genomic state within days. Chronic exposure induced MHC class II gene expression, normally restricted to professional antigen-presenting cells. We validated MHCII protein in primary tissue and hCOs and used co-immunoprecipitation and mass spectrometry to identify candidate antigens. Finally, we showed that exogenous peptides from fetal neurons could be presented by astrocytic MHCII.

neuroscience↗

Computational Identification of Ligand-Receptor Pairs that Drive Human Astrocyte Development

Extrinsic signaling between diverse cell types is crucial to nervous system development. Ligand binding is a key driver of developmental processes, but it remains a significant challenge to disentangle how collections of these signals act cooperatively to affect changes in recipient cells. In the developing human brain, cortical progenitors transition from neurogenesis to gliogenesis in a stereotyped progression that is influenced by extrinsic ligands. Therefore, we sought to use the wealth of published genomic data in the developing human brain to identify and then test novel ligand combinations that act synergistically to drive gliogenesis. Using computational tools, we identified ligand-receptor pairs that are expressed at appropriate developmental stages, in relevant cell types, and whose activation is predicted to cooperatively stimulate complimentary astrocyte gene signatures. We then tested a group of five neuronally-secreted ligands and validated their synergistic contributions to astrocyte development within both human cortical organoids and primary fetal tissue. We confirm cooperative capabilities of these ligands far greater than their individual capacities and discovered that their combinatorial effects converge on AKT/mTOR signaling to drive transcriptomic and morphological features of astrocyte development. This platform provides a powerful agnostic framework to identify and test how extrinsic signals work in concert to drive developmental processes. HIGHLIGHTSO_LIComputational prediction of active ligand-receptor pairs in the developing brain C_LIO_LISynergistic contributions of predicted ligands drive astrocyte development C_LIO_LILigands induce transcriptomic and morphological features of mature astrocytes C_LIO_LICooperative ligand activity converges on AKT/mTOR signaling C_LI

neuroscience↗