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Natural killer cells cooperate with neutrophils to suppress pathological angiogenesis in neovascular age-related macular degeneration [scRNA-seq]

ABSTRACT: Natural killer cells cooperate with neutrophils to suppress pathological angiogenesis in neovascular age-related macular degeneration [scRNA-seq]

PROVIDER: PRJNA1130615 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29673189_1.fastq.gz	Fastqsanger.gz
	SRR29673189_2.fastq.gz	Fastqsanger.gz
	SRR29673190_1.fastq.gz	Fastqsanger.gz
	SRR29673190_2.fastq.gz	Fastqsanger.gz
	SRR29673191_1.fastq.gz	Fastqsanger.gz

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Natural killer cells cooperate with neutrophils to suppress pathological angiogenesis in neovascular age-related macular degeneration

Project description:Natural killer cells cooperate with neutrophils to suppress pathological angiogenesis in neovascular age-related macular degeneration

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Natural killer cells cooperate with neutrophils to suppress pathological angiogenesis in neovascular age-related macular degeneration

Project description:Neovascular age-related macular degeneration (nvAMD) is the leading cause of blindness in the elderly population associated with focal inflammation, however, understanding of the precise immune components governing this process is still limited. Here, we identified natural killer (NK) cells as a prominent lymphocyte population infiltrating the perivascular space of choroidal neovascularization (CNV) lesions. O-link analysis and single-cell RNA sequencing approaches identified CCR5-expressing NK cells is essential for further NK cell recruitment and extravasation in CNV site. NK cells suppress pathological angiogenesis via through clearance of senescent vasculatures, a process that requires neutrophil extracellular traps (NETs). Mechanistically, the release of NETs results from NKG2D-dependent NK cell activation and production of IFN-γ at CNV lesions. Notably , age is the strongest risk factor for AMD to an aged immune system; our human and mouse data showed that aged NK cells exhibited compromised protective effects. Additionally, expansion of NK cells by IL-2 complex improved CNV formation. Collectively, our results revealed a previously unrecognized role of NK cells in suppressing nvAMD progression, suggesting these cells as a potential target for future immune therapies for patients with nvAMD.

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Natural killer cells cooperate with neutrophils to suppress pathological angiogenesis in neovascular age-related macular degeneration [scRNA-seq]

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Total blood monocyte gene expression from neovascular age-related macular degeneration patients and age-matched controls

Project description:Mononuclear phagocytes (MPs), including monocytes and macrophages, play complex roles in the pathogenesis of age-related macular degeneration (AMD). We aimed to perform global transcriptome analysis on monocytes from AMD patients to obtain additional insight to the role of MPs in AMD. Peripheral blood was taken from treatment-naïve neovascular AMD (nvAMD) patients (n=14), and age-matched controls (n=15). Peripheral blood mononuclear cells (PBMCs) were separated and monocytes were isolated via negative selection. Gene expression was evaluated with Affymetrix Gene1.0 ST microarrays. Statistical/bioinformatics analysis was performed using open sourceware programs.

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Impaired RPE Mitochondrial Energetics Leads Subretinal Fibrosis in Neovascular Age-related Macular Degeneration

Project description:Subretinal fibrosis permanently impairs the vision of patients with neovascular age-related macular degeneration. Despite emerging evidence revealing the association between disturbed metabolism in retinal pigment epithelium (RPE) and subretinal fibrosis, the underlying mechanism remains unclear. In the present study, single-cell RNA sequencing revealed, prior to subretinal fibrosis, genes in mitochondrial fatty acid oxidation are downregulated in the RPE lacking very low-density lipoprotein receptor (VLDLR), especially the rate-limiting enzyme carnitine palmitoyltransferase 1A (CPT1A). We found that overexpression of CPT1A in the RPE of Vldlr-/- mice suppresses epithelial-to-mesenchymal transition and fibrosis. Mechanistically, TGFβ2 induces fibrosis by activating a Warburg-like effect, i.e. increased glycolysis and decreased mitochondrial respiration through ERK-dependent CPT1A degradation. Moreover, VLDLR blocks the formation of the TGFβ receptor I/II complex by interacting with unglycosylated TGFβ receptor II. In conclusion, VLDLR suppresses fibrosis by attenuating TGFβ2-induced metabolic reprogramming, and CPT1A is a potential target for treating subretinal fibrosis.

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Macrophage microRNA-150 promotes pathological angiogenesis as seen in age-related macular degeneration

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Macrophage microRNA-150 promotes pathological angiogenesis as seen in age-related macular degeneration: part I

Project description:Macrophage aging is pathogenic in numerous age-associated diseases, including age-related macular degeneration. The purpose of this experiment was to profile microRNA expression in young and aged macrophages at baseline and in response to oxLDL and acLDL.

2018-04-05 | GSE111304 | GEO

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Transcriptomic Characterization of Human Choroidal Neovascular Membranes Identifies Calprotectin as a Novel Biomarker for Patients with Age-related Macular Degeneration

Project description:Although genome-wide association studies, animal models, and cell culture systems have yielded important insights into the pathogenesis of neovascular age-related macular degeneration (nAMD), the underlying molecular pathways remain ill defined. Recent studies have deciphered the transcriptional profile of choroidal neovascularisation (CNV) of body donor eyes and were thus limited by the time span from death to preservation and the associated rapid 5'-RNA degradation. In this study, CNVs were therefore formalin-fixed immediately after surgical extraction from patients with nAMD and analyzed using a 3’ RNA sequencing approach called Massive Analysis of cDNA Ends (MACE). Age-matched formalin-fixed paraffin-embedded (FFPE) RPE-choroidal specimens obtained from the macular region of enucleated eyes with ciliary body melanoma served as controls. Transcriptome profiles were generated and disease-associated gene signatures were identified using statistical and bioinformatic methods. Calprotectin (S100A8/A9) protein expression was investigated by immunohistochemistry and ELISA.We identified 158 differentially-expressed genes (DEG) that were significantly increased in CNV compared to control tissue. Gene ontology enrichment analysis demonstrated that these DEG contributed to biological processes, such as Blood Vessel Development, Extracellular Structure Organization, Response to Wounding and several immune-related terms. The S100 calcium-binding protein A8 (S100A8) and S100A9 emerged among the top DEG, as confirmed by immunohistochemistry on CNV tissue and protein analysis of vitreous samples from nAMD patients and controls. This study provides a high-resolution RNA-sequencing-based transcriptional signature of choroidal neovascular membranes in AMD patients and reveals S100A8/A9 as a novel biomarker and promising target for AMD-directed therapeutics and diagnostics.

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