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Deletion of the Alzheimer’s Disease-associated CD33 results in increased phagocytosis, oxidative burst and inflammation

ABSTRACT: Deletion of the Alzheimer’s Disease-associated CD33 results in increased phagocytosis, oxidative burst and inflammation

PROVIDER: PRJNA650315 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12371410.fastq.gz	Fastqsanger.gz
	SRR12371411.fastq.gz	Fastqsanger.gz
	SRR12371412.fastq.gz	Fastqsanger.gz
	SRR12371413.fastq.gz	Fastqsanger.gz
	SRR12371414.fastq.gz	Fastqsanger.gz

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Deletion of the Alzheimer’s Disease-associated CD33 results in increased phagocytosis, oxidative burst and inflammation

Project description:In this study, wild type and CD33 knockout human THP1 macrophages were treated with control shRNA or shRNA against the CD33 signaling-associated protein tyrosine phosphatase PTPN6 and analyzed by mRNA sequencing. Whole genome transcriptome analysis showed that knockout of CD33 as well as knockdown of PTPN6 led to constitutive activation of inflammation-related pathways. On the other hand, PTPN6 knockdown was associated with changes in cell cycle and mitosis-related pathways in a CD33-deficient background.

2021-01-31 | GSE155567 | GEO

The CD33 short isoform is a gain-of-function variant that enhances Aß1-42 phagocytosis in microglia II

Project description:Background: CD33 is genetically linked to Alzheimer’s disease (AD) susceptibility through differential expression of isoforms in microglia. The role of the human CD33 short isoform (hCD33m), preferentially encoded by an AD-protective CD33 allele (rs12459419T), is unknown. Here, we test whether hCD33m represents a loss-of-function or gain-of-function variant. Results: In both primary microglia and U937 cells, we find that hCD33m enhances phagocytosis. This contrasts with the human CD33 long isoform (hCD33M) that represses phagocytosis, as previously demonstrated. As revealed by scRNAseq, hCD33m+ microglia are enriched in a cluster of cells defined by an upregulated expression and gene regulatory network of immediate early genes, which was further validated within microglia in situ. Using a new hCD33m-specific antibody enabled hCD33m expression to be examined, demonstrating a preference for an intracellular location. Moreover, this newly discovered gain-of-function role for hCD33m is dependent on its cytoplasmic signaling motifs, dominant over hCD33M, and not due to loss of glycan ligand binding. Conclusions: These results provide strong support that hCD33m represents a gain-of-function isoform and offers insight into what it may take to therapeutically capture the AD-protective CD33 allele. We have developed two models to test the role of hCD33m. The first is a new strain of transgenic mice expressing hCD33m in the microglial cell lineage. The second is U937 cells where the CD33 gene was disrupted by CRISPR/Cas9 and complemented with different variants of hCD33. Primary microglia and U937 cells were tested in phagocytosis assays and single cell RNA sequencing (scRNAseq) was carried out on the primary microglia. Furthermore, a new monoclonal antibody was developed to detect hCD33m more efficiently.

2021-04-21 | GSE172527 | GEO

The CD33 short isoform is a gain-of-function variant that enhances Aß1-42 phagocytosis in microglia I

2021-04-21 | GSE172525 | GEO

TREM2 Acts Downstream of CD33 in Modulating Microglial Pathology in Alzheimer's Disease

Project description:CD33-/- and/or TREM2-/- mice were crossed with the 5xFAD mouse model of Alzheimer’s disease to generate single and double CD33/TREM2 knock-out mice on 5xFAD background. Transcriptome and gene expression analyses were performed to analyze the impact of CD33 and/or TREM2 knock-out on the transcriptome of microglia in the context of amyloid pathology. The results revealed that CD33 and/or TREM2 knock-out reprogrammed microglial gene expression signatures in 5xFAD mice in an age-dependent manner. Differential gene expression in 5xFAD;CD33-/- microglia depended on the presence of TREM2. These data suggest that TREM2 acts downstream of CD33.

2019-06-11 | GSE132508 | GEO

RNA expression profiling of CD13/CD33-positive and CD13/CD33-negative B-ALL patients [mRNA expression]

Project description:To study the effect of expression of CD13/CD33 on the pathogenesis of B-cell acute lymphoblastic (B-ALL), we collected samples from 4 CD13/CD33-positive and 4 CD13/CD33-negative B-ALL patients and performed RNA-seq.

2023-12-31 | GSE197178 | GEO

RNA expression profiling of CD13/CD33-positive and CD13/CD33-negative B-ALL patients [miRNA expression]

2023-12-31 | GSE197180 | GEO

The CD33 short isoform is a gain-of-function variant that enhances Aß1-42 phagocytosis in microglia

Project description:The CD33 short isoform is a gain-of-function variant that enhances Aß1-42 phagocytosis in microglia

| PRJNA723594 | ENA

Genome-wide expression profile on hiPSCs and hiPSC-derived CD33+ myeloid cells

Project description:To gain insights into which pathways might be dysregulated in JMML, we compared the transcriptome profiles among hiPSC and sorted CD33+ myeloid cells from control and patient samples. NS/JMML-derived CD33+ myeloid cells showed dysregulation in major biological processes. Moreover, a consistent expression pattern among sets of genes related to pluripotency and myeloid regulation was observed in the control, NS and NS/JMML CD33+ myeloid cells further supporting generally successful myelopoiesis. Total RNA obtained from hiPSC and sorted CD33+ myeloid cells (at day 14 of differentiation) from control and patient samples

2014-01-31 | E-GEOD-54538 | biostudies-arrayexpress

RNA-seq of CD33 KO and control HSPCs

Project description:Gene expression profile of in vitro differentiated control and CD33 KO CD34+ cells (with 70-85% CD33 KO) were analyzed by RNA-seq to exclude any major impact of CD33 loss on downstream gene expression

2018-04-26 | GSE113670 | GEO

The CD33 short isoform is a gain-of-function variant that enhances Aß1-42 phagocytosis in microglia I

Project description:The CD33 short isoform is a gain-of-function variant that enhances Aß1-42 phagocytosis in microglia I

| PRJNA723598 | ENA