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Metabolic reprogramming of the neovascular niche promotes regenerative angiogenesis in proliferative retinopathy

ABSTRACT: Metabolic reprogramming of the neovascular niche promotes regenerative angiogenesis in proliferative retinopathy

PROVIDER: PRJNA894955 | ENA |

REPOSITORIES: ENA

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	SRR22063232_1.fastq.gz	Fastqsanger.gz
	SRR22063232_2.fastq.gz	Fastqsanger.gz
	SRR22063234_1.fastq.gz	Fastqsanger.gz
	SRR22063234_2.fastq.gz	Fastqsanger.gz

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Metabolic reprogramming of the neovascular niche promotes regenerative angiogenesis in proliferative retinopathy

Project description:Healthy blood vessels supply neurons to preserve metabolic function. In blinding proliferative retinopathies (PRs), pathological neovascular tufts often emerge in lieu of needed physiological revascularization. Here we show that metabolic shifts in the neovascular niche define angiogenic fate. Fatty acid oxidation (FAO) metabolites accumulated in human and murine retinopathy samples. Neovascular tufts with a distinct single-cell transcriptional signature highly expressed FAO enzymes. The deletion of Sirt3, an FAO regulator, shifted the neovascular niche metabolism from FAO to glycolysis and suppressed tuft formation. This metabolic transition increased Vegf expression in astrocytes and reprogrammed pathological neovessels to a physiological phenotype, hastening vascular regeneration of the ischemic retina and improving vision. Hence, strategies to change the metabolic environment of vessels could promote a regenerative phenotype in vascular diseases.

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Induced Expression of VEGFC, ANGPT, and EFNB2 and Their Receptors Characterizes Neovascularization in Proliferative Diabetic Retinopathy

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Project description:Diabetic retinopathy (DR) is a leading cause of blindness in adults under 40 in the developed world, with a significant proportion progressing to vision-threatening stages like proliferative diabetic retinopathy (PDR) and neovascular glaucoma (NVG). This study aims to explore the molecular mechanisms underlying the progression from non-proliferative DR (NPDR) to PDR and NVG, focusing on identifying potential biomarkers and therapeutic targets. We utilized discovery-based proteomics, specifically label free quantification (LFQ), to analyze aqueous humor (AH) proteins from patients with NPDR, PDR, and NVG from the AH samples obtained during cataract surgery or anterior chamber paracentesis. We employed triple quadrupole (QQQ)-MS for targeted protein quantification to validate marker proteins for each disease state. Notably,subsequent analyses revealed specific proteins associated with each stage of DR. Gene ontology analysis and functional annotation unveiled significant processes in DR such as immune response and lipid metabolic process. Validation of potential biomarkers revealed proteins showing significant concentration changes, with several candidates demonstrating diagnostic potential through ROC curve analysis. These findings provide insights into the biomarkers and pathogenesis of these severe neovascular complications. The identification of specific proteins associated with the progression of DR to more advanced stages offer a promising avenue for early diagnosis and targeted therapy. The study underscores the potential of AH proteomics in understanding complex diseases like DR and its complications.

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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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