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Gene expression analysis of astrocytes differentiated from iPS cells generated from the fibroblasts of PSEN1deltaE9 mutant AD and their isogenic control iPS lines

ABSTRACT: Gene expression analysis of astrocytes differentiated from iPS cells generated from the fibroblasts of PSEN1deltaE9 mutant AD and their isogenic control iPS lines

PROVIDER: PRJNA576835 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10257345.fastq.gz	Fastqsanger.gz
	SRR10257346.fastq.gz	Fastqsanger.gz
	SRR10257347.fastq.gz	Fastqsanger.gz
	SRR10257348.fastq.gz	Fastqsanger.gz
	SRR10257349.fastq.gz	Fastqsanger.gz

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APOE-isogenic iPSC-derived astrocytes

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Gene expression analysis of astrocytes differentiated from iPS cells generated from the fibroblasts of PSEN1deltaE9 mutant AD and their isogenic control iPS lines

Project description:Mutations in presenilin 1 (PSEN1) cause a familiar form of Alzheimer's disease (AD). We have obtained skin biopsies from two individuals carrying PSEN1 exon9 deletion and reprogrammed skin fibroblasts into induced pluripotent stem cells (iPSCs). To get controls, we have corrected PSEN1 exon9 deletion by CRISPR/Cas9 technique. Since astrocytes play role in AD pathogenesis, we further differentiated iPSCs into astrocytes. We ran RNA sequencing analysis to compare our iPSC-derived astrocytes with previously published data on human astrocytes and to identify genes and pathways affected by PSEN1 exon 9 deletion.

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Gene expression analysis of astrocytes differentiated from iPS cells generated from monozygotic twins discordant for schizophrenia

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in-vitro differentiated midbrain dopaminergic neurons from isogenic human induced pluripotent stem cells

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in-vitro differentiated midbrain dopaminergic neurons from isogenic human induced pluripotent stem cells

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Aberrant neurodevelopment in human iPS cell-derived models of Alexander disease

Project description:Alexander disease (AxD) is a rare, severe neurodegenerative disorder caused by mutations in the glial fibrillary acidic protein (GFAP). While the exact disease mechanism remains unknown, existing studies suggest that the mutant GFAP influences many cellular processes, including cytoskeleton stability, mechanosensing, cell energetics, and proteasome function. While most studies have primarily focused on GFAP-expressing astrocytes, this protein is also expressed by radial glia and neural progenitor cells, prompting questions about the impact of GFAP mutations on central nervous system (CNS) development. In this study, we present an intriguing observation of an impaired differentiation of astrocytes and neurons in co-cultures of astrocytes and neurons, as well as in brain organoids, both generated from patient-derived induced pluripotent stem (iPS) cells with a GFAP (R239C) mutation. Leveraging single-cell RNA sequencing (scRNA-seq), we identified distinct cell populations and transcriptomic changes between the GFAP mutant cells and an isogenic corrected control. These findings are supported with immunocytochemistry and proteomics. In co-cultures, the AxD mutation resulted in an increased abundance of immature cells, while in organoids, we observed an altered cell differentiation and reduced abundance of astrocytes. Additionally, gene expression analysis associated the AxD mutation with increased stress susceptibility, cytoskeletal abnormalities, and altered extracellular matrix and cell-cell communication patterns. Overall, our results suggest the possibility of a faulty differentiation in human iPS cell-derived models of AxD, opening new avenues for AxD research.

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Project description:Apolipoprotein 4 (APOE4), is the strongest genetic risk allele associated with the development of late onset Alzheimer’s disease (AD). Across the CNS, astrocytes are the predominant expressor of Apoe while also being critical mediators of neuroinflammation and cerebral metabolism. APOE4 has been consistently linked with dysfunctional neuro-immunometabolism, however insights into the molecular constituents driving these responses remain unclear. Utilizing complimentary approaches across humanized ApoE expressing mice and isogenic IPS astrocytes, we demonstrate that harboring ApoE4 alters astrocyte immunometabolic response to pro-inflammatory stimuli. Our findings demonstrate that ApoE4-expressing astrocytes acquire distinct transcriptional repertoires at the single-cell and spatially-resolved domains, which driven, in-part, by preferential utilization of the cRel transcription factor. Further, inhibiting cRel translocation abrogated inflammatory-induced glycolytic shift and ultimately resulted in significantly dampened glycolysis-associated metabolites in tandem with mitigating production of multiple pro-inflammatory cytokines. Altogether, our findings elucidate novel cellular underpinnings by which ApoE4 drives maladaptive immunometabolic responses of astrocytes.

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