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Single-cell Transcriptome Analyses Reveal Unique Microglia Types Associated with Retinal Pathological Angiogenesis

ABSTRACT: Single-cell Transcriptome Analyses Reveal Unique Microglia Types Associated with Retinal Pathological Angiogenesis

PROVIDER: PRJNA821499 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18539920.fastq.gz	Fastqsanger.gz
	SRR18539921.fastq.gz	Fastqsanger.gz
	SRR18539922.fastq.gz	Fastqsanger.gz
	SRR18539923.fastq.gz	Fastqsanger.gz
	SRR18539924.fastq.gz	Fastqsanger.gz

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Single-cell Transcriptome Analyses Reveal Unique Microglia Types Associated with Retinal Pathological Angiogenesis

Project description:We used single cell RNA-seq to comprehensively map all retinal microglia populations in a mouse model of oxygen-induced PR. We unveiled several unique types of PR-associated microglia (PRAM) and identified markers, signaling pathways, and regulons associated with these cells. Among these microglial subpopulations, we found a highly proliferative subset of cells with a high self-renewal capacity and a subset of cells with hypermetabolism that expresses high levels of activating microglia markers, glycolytic enzymes, and pro-angiogenic insulin-like growth factor 1. Immunohistochemical staining shows that PRAMs were spatially located within neovascular tufts. These unique microglial subtypes have the potential to promote retinal angiogenesis, which may have important implications for the future treatment of PR and other ocular diseases characterized by pathological angiogenesis.

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Role of microRNA-143, -150 and 126 in pathological retinal angiogenesis

Project description:Retinal neovascularization is a severe complication of proliferative diabetic retinopathy. We have previously identified that miRNAs is directly involved in the development of retinal neovascularization. Here, we explored the role of miRNAs and its underlying mechanism in modulating angiogenesis.

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BGN stimulates retinal pathological angiogenesis via up-regulation of CXCL12 expression in pericytes (mouse)

Project description:Retinal pathological angiogenesis (PA) is a common hallmark in proliferative retinopathies, including age-related macular degeneration (AMD), proliferative diabetic retinopathy (PDR), and retinopathy of prematurity (ROP). The mechanisms underlying PA is complex and incompletely understood. Using oxygen-induced retinopathy (OIR) mouse as a model, the role of extracellular matrix (ECM) protein biglycan (BGN) in PA was studied. Significant upregulation of BGN in the retina of OIR mice and in neovascular proliferative membranes of PDR patients was found. The reduction of BGN expression by Bgn-specific small interfering RNA (siRNA) effectively diminished retinal PA in OIR mouse. Subsequent analysis of the mouse OIR retinal single-cell RNA sequencing data from the Gene Expression Omnibus dataset (GSE150703) suggested pericyte as a source of BGN. This was verified using cultured retinal capillary pericytes. BGN expression in pericytes was highly sensitive to hypoxic stimulation. BGN stimulated retinal PA via the upregulation of C-X-C motif chemokine ligand 12 (CXCL12). Inhibition of the CXCL12-CXCR4 axis effectively diminished PA in OIR mouse. In conclusion, this study demonstrated the stimulatory role of BGN in retinal PA, identified the link between BGN and CXCL12 expression, and further highlighted the role of pericytes in retinal PA.

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BGN stimulates retinal pathological angiogenesis via up-regulation of CXCL12 expression in pericytes (human)

2025-02-10 | GSE259254 | GEO

BGN stimulates retinal pathological angiogenesis via up-regulation of CXCL12 expression in pericytes

Project description:BGN stimulates retinal pathological angiogenesis via up-regulation of CXCL12 expression in pericytes

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COCO/DAND5 inhibits developmental and pathological ocular angiogenesis

Project description:Neovascularization contributes to multiple visual disorders including age-related macular degeneration (AMD). Current therapies for treating ocular angiogenesis are centered on the inhibition of vascular endothelial growth factor (VEGF). While clinically effective, some AMD patients are refractory or develop resistance to anti-VEGF and concerns of increased risks of developing geographic atrophy following long-term treatment have been raised. Identification of alternative pathways to inhibit pathological angiogenesis is thus important. We have identified a novel inhibitor of angiogenesis, COCO/DAND5, a member of the Cerberus-related DAN family. We demonstrate that COCO inhibits sprouting, migration and cellular proliferation of cultured endothelial cells. Intravitreal injections of COCO inhibited retinal vascularization during development and in models of retinopathy of prematurity and AMD. COCO equally abrogated angiogenesis in choroid explants and in a model of choroidal neovascularization. Mechanistically, COCO inhibited the expression of TGFβ and BMP pathwaysand altered ATP production, glucose uptake and redox balance of endothelial cells. Together, these data show that COCO is an inhibitor of retinal and choroidal angiogenesis, possibly representing a therapeutic option for the treatment of neovascular ocular diseases.

2020-12-22 | GSE160099 | GEO

BGN stimulates retinal pathological angiogenesis via up-regulation of CXCL12 expression in pericytes (mouse)

Project description:BGN stimulates retinal pathological angiogenesis via up-regulation of CXCL12 expression in pericytes (mouse)

| PRJNA1080537 | ENA

BGN stimulates retinal pathological angiogenesis via up-regulation of CXCL12 expression in pericytes (human)

Project description:BGN stimulates retinal pathological angiogenesis via up-regulation of CXCL12 expression in pericytes (human)

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Glutamatergic neuronal activity regulates retinal angiogenesis and blood-retinal barrier via Norrin/b-catenin signaling

Project description:Interactions among neuroglial and vascular components are crucial for retinal angiogenesis and blood-retinal barrier (BRB) maturation. Neuronal synaptic dysfunctions precede vascular abnormalities in many retinal pathologies. However, whether neuronal activity, specifically glutamatergic activity, regulates retinal angiogenesis and BRB maturation remains unclear. Using in vivo genetic studies in mice, single-cell RNA-sequencing and functional validation, we found that deep plexus angiogenesis and paracellular BRB maturation are delayed in Vglut1-/- retinas, where neurons fail to release glutamate. In contrast, deep plexus angiogenesis and paracellular BRB maturation are accelerated in Gnat1-/- retinas, where constitutively depolarized rods release excess glutamate. Mechanistically, Norrin expression and endothelial Norrin/b-catenin signaling are downregulated in Vglut1-/- retinas, and upregulated in Gnat1-/- retinas. Pharmacological activation of endothelial Norrin/ b-catenin signaling in Vglut1-/- retinas rescued both deep plexus angiogenesis and paracellular BRB integrity. Thus, our findings demonstrate that glutamatergic neuronal activity regulates retinal angiogenesis and BRB maturation by modulating Norrin/b-catenin signaling.

2024-06-27 | GSE235993 | GEO

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