Next-generation sequencing of control and schizophrenia hiPSC derived NPC
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA358684 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5128180.fastq.gz | Fastqsanger.gz | |||
| SRR5128190.fastq.gz | Fastqsanger.gz | |||
| SRR5128181.fastq.gz | Fastqsanger.gz | |||
| SRR5128191.fastq.gz | Fastqsanger.gz | |||
| SRR5128182.fastq.gz | Fastqsanger.gz |
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Project description:We report the genome-wide binding patterns of nuclear FGFR1 in Control and Schizophrenia hiPSC-dervied NPC differntiated in neuronal media for two days. We also report the genome-wide binding patterns of NOTCH in schizophrenia hiPSC-dervied NPC differntiated in neuronal media for 2 days
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Project description:We Report the genome-wide RNA expression levels in control and schizophrenia hiPSC dervied NPC treated with neuronal media for 2 days. In total about 15,000 gene expression were detected in all samples, of which 1349 were dysregualted.
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Project description:We Report the genome-wide RNA expression levels in control and schizophrenia hiPSC dervied NPC treated with neuronal media for 2 days. In total, 440 microRNA expression were detected in all samples, of which 16 were dysregualted.
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Project description:Cell-based models of many neurological and psychiatric diseases, established by reprogramming patient somatic cells into human induced pluripotent stem cells (hiPSCs), have now been reported. While numerous reports have demonstrated that neuronal cells differentiated from hiPSCs are electrophysiologically active mature neurons, the âageâ of these cells relative to cells in the human brain remains unresolved. Comparisons of gene expression profiles of hiPSC-derived neural progenitor cells (NPCs) and neurons to the Allen BrainSpan Atlas indicate that hiPSC neural cells most resemble first trimester neural tissue. Consequently, we posit that hiPSC-derived neural cells may most accurately be used to model the early developmental defects that contribute to disease predisposition rather than the late features of the disease. Though the characteristic symptoms of schizophrenia SZ generally appear late in adolescence, it is now thought to be a neurodevelopmental condition, often predated by a prodromal period that can appear in early childhood. Postmortem studies of SZ brain tissue typically describe defects in mature neurons, such as reduced neuronal size and spine density in the prefrontal cortex and hippocampus, but abnormalities of neuronal organization, particularly in the cortex, have also been reported. We postulated that defects in cortical organization in SZ might result from abnormal migration of neural cells. To test this hypothesis, we directly reprogrammed fibroblasts from SZ patients into hiPSCs and subsequently differentiated these disorder-specific hiPSCs into NPCs. SZ hiPSC differentiated into forebrain NPCs have altered expression of a number of cellular adhesion genes and WNT signaling. Methods: We compared global transcription of forebrain NPCs from six control and four SZ patients by RNAseq. Results: Multi-dimensional scaling (MDS) resolved most SZ and control hiPSC NPC samples; 848 genes were significantly differentially expressed (FDR<0.01) Conclusions: The WNT signaling pathway was enriched 2-fold (fisher exact test p-value = 0.031). 1-2 independent differentiations (biological replicates) for each of four control and four schizophrenia patients were analyzed; samples were generated in parallel to neuron RNAseq data.
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Project description:Cell-based models of many neurological and psychiatric diseases, established by reprogramming patient somatic cells into human induced pluripotent stem cells (hiPSCs), have now been reported. While numerous reports have demonstrated that neuronal cells differentiated from hiPSCs are electrophysiologically active mature neurons, the “age” of these cells relative to cells in the human brain remains unresolved. Comparisons of gene expression profiles of hiPSC-derived neural progenitor cells (NPCs) and neurons to the Allen BrainSpan Atlas indicate that hiPSC neural cells most resemble first trimester neural tissue. Consequently, we posit that hiPSC-derived neural cells may most accurately be used to model the early developmental defects that contribute to disease predisposition rather than the late features of the disease. Though the characteristic symptoms of schizophrenia SZ generally appear late in adolescence, it is now thought to be a neurodevelopmental condition, often predated by a prodromal period that can appear in early childhood. Postmortem studies of SZ brain tissue typically describe defects in mature neurons, such as reduced neuronal size and spine density in the prefrontal cortex and hippocampus, but abnormalities of neuronal organization, particularly in the cortex, have also been reported. We postulated that defects in cortical organization in SZ might result from abnormal migration of neural cells. To test this hypothesis, we directly reprogrammed fibroblasts from SZ patients into hiPSCs and subsequently differentiated these disorder-specific hiPSCs into NPCs. SZ hiPSC differentiated into forebrain NPCs have altered expression of a number of cellular adhesion genes and WNT signaling. Methods: We compared global transcription of forebrain NPCs from six control and four SZ patients by RNAseq. Results: Multi-dimensional scaling (MDS) resolved most SZ and control hiPSC NPC samples; 848 genes were significantly differentially expressed (FDR<0.01) Conclusions: The WNT signaling pathway was enriched 2-fold (fisher exact test p-value = 0.031).
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Project description:Extracellular vesicles (EVs) are tiny membranous structures capable of mediating intercellular communication. In the brain, the role(s) of EVs have been extensively studied in the context of neurological diseases, but their potential implications in the neuropathology underlying human mental disorders remain largely unexplored. Here, we investigated the potential role(s) of brain EVs in schizophrenia (SZ) by analyzing these vesicles from the three post-mortem anatomical brain regions: prefrontal cortex (PFC), hippocampus (HC) and caudate (CAU), using next-generation discovery-driven proteomics. Our results indicate that EVs from SZ-affected brains present region-specific proteins associated with abnormal GABAergic and glutamatergic transmission, as well as alterations in proteins involved in synaptic decay, abnormal brain immunity, neuronal structural imbalances and impaired cell homeostasis. Our findings also provide the first evidence that molecular exchange networks are potentially active and mediated by EVs in cognitively healthy brains. These EV-mediated networks were partially reversed and largely disrupted in brains affected by SZ.
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Project description:Schizophrenia is a severe and debilitating neuropsychiatric disorder with the involvement of genetic and environmental factors contributing to its pathogenesis. The specific role of the brain cell types in the disease remains uncovered due to the difficulties in accessing diseased tissue. This study analysed molecular alterations in human induced pluripotent stem cells derived from fibroblasts from control subject and individual with schizophrenia and further differentiated to neuron to identify genes relevant for the development of schizophrenia. We identified 228 genes that are involved with metabolic processes, signal transduction, nervous system development, regulation of neurogenesis and neuronal differentiation. These genes were analysed in expression microarrays of post-mortem brain tissue (frontal cortex) of additional patients with schizophrenia and normal individuals revealing only six common genes: CACNA1E, CEBPB, DUX4, EDNRA, SPHK1 and SPRY4. Furthermore, a co-expression network analysis of the 228 genes revealed a non-conserved module enriched for genes associated with oxidative stress and negative regulation of cell differentiation as involved with schizophrenia. This study supports the relevance of using cellular approaches to dissect molecular aspects of neurogenesis with impact in the schizophrenic brain. Biopsies of primary human fibroblasts from a 48-year-old woman with DSM-IVTR schizophrenia defined as treatment-resistant under clozapine treatment (SZCP) were collected in parallel with a control subject (CON) negative for any major lifetime DSM-IVTR diagnosis. Fibroblasts underwent primary culture procedures to generate hiPSCs and were subsequently differentiated into neurons (NPC). Samples generation and culture conditions are described in Paulsen et al. (2011). Five replicates of expression microarray experiments using a reference design, where test sample (NPC) is derived from reference sample (hiPSC).
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