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Multi-omic comparison of Alzheimer’s variants in human ESC-derived microglia reveals convergence at APOE [ChIP-seq]

ABSTRACT: Multi-omic comparison of Alzheimer’s variants in human ESC-derived microglia reveals convergence at APOE [ChIP-seq]

PROVIDER: PRJNA643558 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12129900.fastq.gz	Fastqsanger.gz
	SRR12129859.fastq.gz	Fastqsanger.gz
	SRR12129860.fastq.gz	Fastqsanger.gz
	SRR12129861.fastq.gz	Fastqsanger.gz
	SRR12129862.fastq.gz	Fastqsanger.gz

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Multi-omic comparison of Alzheimer’s variants in human ESC-derived microglia reveals convergence at APOE

Project description:Multi-omic comparison of Alzheimer’s variants in human ESC-derived microglia reveals convergence at APOE

| PRJNA643555 | ENA

Multi-omic comparison of Alzheimer’s variants in human ESC-derived microglia reveals convergence at APOE [ChIP-seq]

Project description:Variations in many genes linked to sporadic Alzheimer’s disease (AD), show abundant expression in microglia, however, relationships between these genes remain largely elusive. Here, we establish isogenic human ES-derived microglia-like cell lines (hMGLs) harboring AD variants in CD33, INPP5D, SORL1 and TREM2 loci, and curate a comprehensive atlas comprising ATACseq, ChIPseq, RNAseq and proteomics datasets. AD-like expression signatures are observed in AD mutant SORL1 and TREM2 hMGLs, while integrative multi-omic analysis of combined epigenetic and expression datasets indicates upregulation of APOE as a convergent pathogenic node. We also observe cross-regulatory relationships between SORL1 and TREM2, where SORL1R744X hMGLs induce TREM2 expression to enhance APOE expression. AD-associated SORL1 and TREM2 mutations also impaired hMGL Aβ uptake in an APOE-dependent manner in vitro, and attenuated Aβ uptake/clearance in mouse AD brain xenotransplants. Utilizing this modeling and analysis platform for human microglia, we provide new insight into epistatic interactions in AD genes and demonstrate convergence of microglial AD genes at the APOE locus.

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Multi-omic comparison of Alzheimer’s variants in human ESC-derived microglia reveals convergence at APOE [ATAC-seq]

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Multi-omic comparison of Alzheimer’s variants in human ESC-derived microglia reveals convergence at APOE [RNA-seq]

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Multi-omic comparison of Alzheimer’s variants in human ESC-derived microglia reveals convergence at APOE [ATAC-seq]

Project description:Multi-omic comparison of Alzheimer’s variants in human ESC-derived microglia reveals convergence at APOE [ATAC-seq]

| PRJNA643557 | ENA

Multi-omic comparison of Alzheimer’s variants in human ESC-derived microglia reveals convergence at APOE [RNA-seq]

Project description:Multi-omic comparison of Alzheimer’s variants in human ESC-derived microglia reveals convergence at APOE [RNA-seq]

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Multi-omic comparison of Alzheimers variants in human ESC-derived microglia reveals convergence at APOE

Project description:Variations in many genes linked to sporadic Alzheimers disease (AD), show abundant expression in microglia, however, relationships between these genes remain largely elusive. Here, we establish isogenic human ES-derived microglia-like cell lines (hMGLs) harboring AD variants in CD33, INPP5D, SORL1 and TREM2 loci, and curate a comprehensive atlas comprising ATACseq, ChIPseq, RNAseq and proteomics datasets. AD-like expression signatures are observed in AD mutant SORL1 and TREM2 hMGLs, while integrative multi-omic analysis of combined epigenetic and expression datasets indicates upregulation of APOE as a convergent pathogenic node. We also observe cross-regulatory relationships between SORL1 and TREM2, where SORL1R744X hMGLs induce TREM2 expression to enhance APOE expression. AD-associated SORL1 and TREM2 mutations also impaired hMGL A-beta uptake in an APOE-dependent manner in vitro, and attenuated A-beta uptake/clearance in mouse AD brain xenotransplants. Utilizing this modeling and analysis platform for human microglia, we provide new insight into epistatic interactions in AD genes and demonstrate convergence of microglial AD genes at the APOE locus

2020-07-07 | MSV000085698 | MassIVE

Multi-omic comparison of Alzheimer’s variants in human ESC-derived microglia reveals convergence at APOE

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-09-01 | GSE153658 | GEO

Multi-omic comparison of Alzheimer's variants in human ESC-derived microglia reveals convergence at APOE.

Project description:Variations in many genes linked to sporadic Alzheimer's disease (AD) show abundant expression in microglia, but relationships among these genes remain largely elusive. Here, we establish isogenic human ESC-derived microglia-like cell lines (hMGLs) harboring AD variants in CD33, INPP5D, SORL1, and TREM2 loci and curate a comprehensive atlas comprising ATAC-seq, ChIP-seq, RNA-seq, and proteomics datasets. AD-like expression signatures are observed in AD mutant SORL1 and TREM2 hMGLs, while integrative multi-omic analysis of combined epigenetic and expression datasets indicates up-regulation of APOE as a convergent pathogenic node. We also observe cross-regulatory relationships between SORL1 and TREM2, in which SORL1R744X hMGLs induce TREM2 expression to enhance APOE expression. AD-associated SORL1 and TREM2 mutations also impaired hMGL Aβ uptake in an APOE-dependent manner in vitro and attenuated Aβ uptake/clearance in mouse AD brain xenotransplants. Using this modeling and analysis platform for human microglia, we provide new insight into epistatic interactions in AD genes and demonstrate convergence of microglial AD genes at the APOE locus.

| S-EPMC7953740 | biostudies-literature

APOE from astrocytes restores Alzheimer’s Aβ-pathology and DAM-like responses in APOE deficient microglia

Project description:The major genetic risk factor for Alzheimer’s disease (AD), APOE4, accelerates beta-amyloid (Aβ) plaque formation, but whether this is caused by APOE expressed in microglia or astrocytes is debated. We express here the human APOE isoforms in astrocytes in an Apoe-deficient AD mouse model. This is not only sufficient to restore the amyloid plaque pathology but also induces the characteristic transcriptional pathological responses in Apoe-deficient microglia surrounding the plaques. We find that both APOE4 and the protective APOE2 from astrocytes increase fibrillar plaque deposition, but differentially affect soluble Aβ aggregates. Microglia and astrocytes show specific alterations in function of APOE genotype expressed in astrocytes. Our experiments indicate a central role of the astrocytes in APOE mediated amyloid plaque pathology and in the induction of associated microglia responses.

2024-10-04 | GSE252454 | GEO

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