Bulk transcriptomic comparison between in vitro propagated DNGR-1-lineage traced cells and hippocampus derived neural stem cells
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ABSTRACT: We compared by bulk RNA sequencing the transcriptomic profile of in vitro cultured DNGR-1-traced neural stem cells or their differentiated astrocytic progeny with similar cell fates generated from bonafide neural stem cells derived from the hippocampus.
Project description:Stem cells are defined by two cardinal properties: limitless self-renewal and multipotency. We have serendipitously found that non-haematopoietic DNGR-1 lineage traced cells residing in the ependymal cell layer of the central nervous system display the two cardinal properties of stem cells, both in vitro and in vivo. However, whether these properties were a feature of all DNGR-1-traced cells or were confined to a particular subset of these is unclear. To address the potential heterogeneity of DNGR-1-traced ependymal cells and caractherise their putative stem cell compartment we conducted single-cell RNA sequencing of DNGR-1-traced cells isolated from uninjured spinal cords.
Project description:Using CD133 as a pan-ependymal cell marker, we wished to understand whether CD133+ DNGR-1 traced cells constituted a distinct subset of ependymal cells by comparing these at the single cell level with CD133+ non-traced cells purified from spinal cords of DNGR-1 lineage tracer mice.
Project description:CD141+DNGR-1+ cDC1 have a dual origin. Both MLP and CMP can differentiate in CD141+DNGR-1+ cDC1s. Using Affymetrix microarrays (GeneChip Human Gene 2.0 ST) we compared gene expression of CD141+DNGR-1+ cDC1s originating either from MLPs or CMPs
Project description:DNGR-1 is a dead cell-sensing receptor specifically expressed in type 1 conventional dendritic cells (cDC1s), but whether it plays a role in antitumor immunity remains unexplored. In our work we have explored the transcriptional profile of tumor-infiltrating cDC1s competent or deficient in DNGR-1,
Project description:VSMCs expressing SCA1 have increased proliferative capacity (Dobnikar et al, 2018; Worssam et al, 2022; Pan et al, 2020). We therefore, mapped chromatin accessibility changes using bulk ATAC-seq for SCA1+ and SCA1- lineage traced VSMCs.