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Transcriptional changes consistent with altered neuronal differentiation, angiogenesis, and tumor plasticity induced in human subpallial telencephalic organoid-glioblastoma chimeras

ABSTRACT: Transcriptional changes consistent with altered neuronal differentiation, angiogenesis, and tumor plasticity induced in human subpallial telencephalic organoid-glioblastoma chimeras

PROVIDER: PRJNA976623 | ENA |

REPOSITORIES: ENA

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Transcriptional changes consistent with altered neuronal differentiation, angiogenesis, and tumor plasticity induced in human subpallial telencephalic organoid-glioblastoma chimeras

Project description:Glioblastoma multiforme (GBM) is one of the most aggressive and therapy-resistant brain tumors prevalent in both adults and children. Despite extensive research to understand GBM pathology, it remains unclear how neural cells in the human brain interact with GBM cells to support their brain propagation and therapy resistance and whether GBM cells exert any influence on the properties of human neural cells. In this study, we co-culture human stem cell-derived subpallial telencephalic organoids with patient-derived proneural or mesenchymal GBM spheroids to investigate their reciprocal interactions. We show that both proneural and mesenchymal GBM spheroids readily fuse and propagate with human organoids, forming organoid-GBM chimeras, without the need for exogenous growth factors. GBM cells within the chimeras adapt by modulating gene expression profiles consistent with diminished proliferation, heightened hypoxia, increased angiogenesis, and proneural-to-mesenchymal transition in proneural GBM. Both proneural or mesenchymal GBMs also exert an impact on the properties of neural cells in the chimeras, leading to the suppression of neuronal genes and an upregulation expression of genes associated with hypoxia and angiogenesis. Collectively, this study identifies specific genes and molecular pathways that can be altered in GBM and neural cells by reciprocal interactions in a human developing brain-like environment for an increased understanding of GBM pathology and future therapy development.

2024-05-25 | GSE233532 | GEO

Human telencephalic organoid development in the presence and absence of exogenous extracellular matrix

Project description:Long-term culture of human telencephalic organoids cultured in the presence or absence of exogenous ECM. To evaluate how ECM supplementation influences organoid development, we supplied exogenous ECM in the form of Matrigel at the beginning of neuroepithelialisation (day 10, D10), either as a solid droplet that provides long-term exposure to a polymerized network of ECM proteins (droplet embedding - condition "drop" in the metadata table), or transiently dissolved in the culture medium (concentration of 2%V/V ) from D10 to D13 (liquid embedding - "liq"). These protocols were compared to one without exposure to exogenous ECM ("no"). Organoids were processed at 120 days of culture, when mature cortical tissue is present.

2023-10-25 | GSE220085 | GEO

Human telencephalic organoid development in the presence and absence of exogenous extracellular matrix

Project description:Human telencephalic organoid development in the presence and absence of exogenous extracellular matrix

| PRJNA908783 | ENA

Single-cell RNA-seq of telencephalic organoids from healthy CTRL and HD (Huntington’s disease) hESC (RUES2) grown as mono-culture or co-culture of chimeric organoids

Project description:Use of single-cell transcriptomics to test early HD selective vulnerability by comparing CTRL and HD telencephalic organoids at day 45 and 120 of differentiation. To test the influence and the interactions between healthy and HD cells, chimeric organoids composed of CTRL and HD cells juxtaposed within the same organoid were grown and analyzed by scRNAseq at day 120.

2024-07-02 | E-MTAB-12924 | biostudies-arrayexpress

TGFβ superfamily signaling regulates the state of human stem cell pluripotency and competency to create telencephalic organoids

Project description:Telencephalic organoids generated from human pluripotent stem cells (hPSC) are emerging as an effective system to study the distinct features of the developing human brain and the underlying causes of many neurological disorders. While progress in organoid technology has been steadily advancing, many challenges remain including rampant batch-to-batch and cell line-to-cell line variability and irreproducibility. Here, we demonstrate that a major contributor to successful cortical organoid production is the manner in which hPSC are maintained prior to differentiation. Optimal results were achieved using fibroblast-feeder-supported hPSC compared to feeder-independent cells, related to differences in their transcriptomic states. Feeder-supported hPSC display elevated activation of diverse TGFβ superfamily signaling pathways and increased expression of genes associated with naïve pluripotency. We further identify combinations of TGFβ-related growth factors that are necessary and together sufficient to impart broad telencephalic organoid competency to feeder-free hPSC and enable reproducible formation of brain structures suitable for disease modeling.

2020-01-01 | GSE140057 | GEO

Modeling human telencephalic development and autism-associated SHANK3 deficiency using organoids generated from single neural rosettes [scRNA-seq]

Project description:Human telencephalon is an evolutionary advanced brain structure associated with many uniquely human behaviors and disorders. However, cell lineages and molecular pathways implicated in human telencephalic development remains largely unknown. We generated human telencephalic organoids from stem cell-derived single neural rosettes (SNRs) and investigated telencephalic development under normal and pathological conditions. SNR-derived organoids contained pallial and subpallial neural progenitors (NPs), excitatory and inhibitory neurons, as well as macroglial and periendothelial cells, and demonstrated predictable organization and cytoarchitecture. We comprehensively characterized the properties of neurons in SNR-derived organoids and identified transcriptional programs associated with the specification of+B50:B51 excitatory and inhibitory lineages from a common pool of NPs early in telencephalic development. We also demonstrated that neurons in organoids with a hemizygous deletion of an autism- and intellectual disability associated gene SHANK3 exhibit intrinsic and excitatory synaptic deficits associated with impaired expression of clustered protocadherins. Collectively, this study validates SNR-derived organoids as a reliable new model for studying human telencephalic development and identifies novel molecular pathways disrupted by SHANK3 hemizygosity in human telencephalic tissue.

2022-08-11 | GSE118697 | GEO

Expression data from Tregs purified from WT-CD3KO or IIKO-CD3KO chimeras

Project description:Disruption of TCR /MHC class II interactions leads rapidly to alterations of the common CD4 Treg transcriptional signature Self-deprived, non-functional Tregs were compare to fully functional Tregs by microarrays. CD3ε-/- mice were lethally irradiated and their immune system reconstituted with WT mouse (WT-CD3KO chimeras) or IIKO mouse (IIKO-CD3KO) Bone Marrow cells. Twenty eight days later, peripheral Tregs from these chimeras were purified for RNA extraction and hybridization on Affymetrix microarrays.

2011-02-09 | E-GEOD-27151 | biostudies-arrayexpress

Modeling human telencephalic development and autism-associated SHANK3 deficiency using organoids generated from single neural rosettes [bulk RNA-seq2]

Project description:Human telencephalon is an evolutionary advanced brain structure associated with many uniquely human behaviors and disorders. However, cell lineages and molecular pathways implicated in human telencephalic development remains largely unknown. We generated human telencephalic organoids from stem cell-derived single neural rosettes (SNRs) and investigated telencephalic development under normal and pathological conditions. SNR-derived organoids contained pallial and subpallial neural progenitors (NPs), excitatory and inhibitory neurons, as well as macroglial and periendothelial cells, and demonstrated predictable organization and cytoarchitecture. We comprehensively characterized the properties of neurons in SNR-derived organoids and identified transcriptional programs associated with the specification of excitatory and inhibitory lineages from a common pool of NPs early in telencephalic development. We also demonstrated that neurons in organoids with a hemizygous deletion of an autism- and intellectual disability associated gene SHANK3 exhibit intrinsic and excitatory synaptic deficits associated with impaired expression of clustered protocadherins. Collectively, this study validates SNR-derived organoids as a reliable new model for studying human telencephalic development and identifies novel molecular pathways disrupted by SHANK3 hemizygosity in human telencephalic tissue.

2022-08-23 | GSE211878 | GEO

Modeling human telencephalic development and autism-associated SHANK3 deficiency using organoids generated from single neural rosettes [bulk RNA-seq1]

2022-08-11 | GSE210959 | GEO

Bulk RNA-seq of MilliporeSigma 3DGro human patient-derived gastrointestinal organoid lines compared to SCC300 human iPSC-derived colon organoid line

Project description:Transcriptomic profiles of 6 commercially-available human patient-derived gastrointestinal organoid lines were obtained and compared to transcriptomic profile of a commercially available human iPSC-induced colon organoid line. Transcriptomic profile of iPSC-derived human colon organoid line was compared after culture in either Corning growth-factor-reduced Matrigel (Corning 356231) or MilliporeSigma growth-factor-reduced ECMGel (E6909)

2022-03-31 | E-MTAB-11557 | biostudies-arrayexpress

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