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Dysregulation of microbiota gut-retina axis in neovascular age-related macular degeneration: beneficial ocular effects of a lutein, zeaxanthin and saffron based prebiotic supplementation

ABSTRACT: This work investigates the effects of a prebiotic mix containing lutein, zeaxanthin, and saffron, recognized for their anti-inflammatory properties, on ophthalmological and microbial parameters in neovascular AMD (nAMD) patients.

ORGANISM(S): human feces metagenome

PROVIDER: GSE261732 | GEO | 2024/12/05

REPOSITORIES: GEO

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Dysregulation of microbiota gut-retina axis in neovascular age-related macular degeneration: beneficial ocular effects of a lutein, zeaxanthin and saffron based prebiotic supplementation

Project description:Dysregulation of microbiota gut-retina axis in neovascular age-related macular degeneration: beneficial ocular effects of a lutein, zeaxanthin and saffron based prebiotic supplementation

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Molecular biomarkers of neovascular age-related macular degeneration with incomplete response to anti-vascular endothelial growth factor treatment

Project description:The standard treatment for neovascular age-related macular degeneration (nAMD) consists of intravitreal anti-vascular endothelial growth factors (VEGF). However, for some patients, even maximal anti-VEGF treatment does notentirely suppress exudative activity. The goal of this study was to identify molecular biomarkers in nAMD with incomplete response to anti-VEGF treatment. Aqueous humor (AH) samples were collected from three groups of patients: 18 patients with nAMD responding incompletely to anti-VEGF, 19 patients affected by nAMD with normal treatment response, and 14 control patients without any retinopathy. Proteomic and multiplex analyses were performed on these samples. Proteomic analyses showed that nAMD patients with incomplete anti-VEGF response displayed an increased inflammatory response, complement activation, cytolysis, protein-lipid complex, and vasculature development pathways. Multiplex analyses revealed a significant increase of soluble vascular cell adhesion molecule-1 (sVCAM-1) [p=0.001], interleukin-6 (IL-6) [p=0.009], bioactive interleukin-12 (IL-12p40) [p=0.03], plasminogen activator inhibitor type 1 (PAI-1) [p=0.004], and hepatocyte growth factor (HGF)[p=0.004] levels in incomplete responders in comparison to normal treatment response. Interestingly, The same biomarkers showed a high intercorrelation with r2 values between 0.58 and 0.94. In addition, we confirmed by AlphaLISA the increase of sVCAM-1 [p<0.0001] and IL-6 [p=0.043] in incomplete responder group. Incomplete responders in nAMD are associated with activated angiogenic and inflammatory pathways. The residual exudative activity of nAMD despite maximal anti-VEGF treatment may be related to both angiogenic and inflammatory responses requiring specific adjuvant therapy.

2021-01-18 | PXD022471 | Pride

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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Role of NR4A1 and non-classical monocytes in a mouse model of neovascular age-related macular degeneration

Project description:Neovascular AMD (nAMD) causes vision loss from destructive angiogenesis, termed choroidal neovascularization (CNV). Cx3cr1-/- mice display non-classical monocyte and microglia alterations, and increased CNV size, suggesting that non-classical monocytes may inhibit CNV formation. While Nr4a1-/- mice are deficient in non-classical monocytes, results are confounded by macrophage hyper-activation. Nr4a1se2/se2 mice lack a transcriptional activator, resulting in non-classical monocyte loss, without macrophage hyper-activation. We subjected Nr4a1-/- and Nr4a1se2/se2 mice to the laser-induced CNV model and performed multi-parameter flow cytometry. We found that both models lack non-classical monocytes, but only Nr4a1-/- mice displayed increased CNV area. Additionally, CD11c+ macrophages were increased in Nr4a1-/- mice. Single-cell transcriptomic analysis uncovered that CD11c+ macrophages were enriched from Nr4a1-/- mice and expressed a pro-angiogenic transcriptomic profile that was disparate from prior reports of macrophage hyper-activation. These results suggest that non-classical monocytes are dispensable during laser-induced CNV, and NR4A1 deficiency shifts the transcriptional profile toward a pro-angiogenic phenotype.

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Dopamine D2 receptor activation inhibits choroidal neovascularization in Parkinson patients with age related macular degeneration.

Project description:Neovascular age-related macular degeneration (nAMD) remains a major cause of visual impairment and puts considerable burden on patients and health care systems. L-DOPA-treated Parkinson Disease (PD) patients have been shown to be partially protected from nAMD, but the mechanism remains unknown. Using murine models combining 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD and laser-induced nAMD, standard PD treatment of L-DOPA/DOPA-decarboxylase inhibitor, or specific dopamine receptor inhibitors, we here demonstrate that L-DOPA treatment-induced increase of dopamine receptor D2 (DRD2) signaling inhibits choroidal neovascularization independently of MPTP-associated nigrostriatal pathway lesion. Analyzing a retrospective cohort of more than two hundred thousand nAMD patients receiving anti-VEGF treatment from the French nationwide insurance database, we show that DRD2-agonist treated (PD) patients have a significantly delayed age of onset for nAMD (81.4 (±7.0) vs 79.4 (±8.1) years old, respectively, p<0.0001) and reduced need for anti-VEGF therapies (-0.6 injections per 100 mg/day daily dose of DRD2 agonists the second year of treatment), similar to the L-DOPA treatment. While providing a mechanistic explanation for an intriguing epidemiological observation, our findings suggest that systemic DRD2 agonists might constitute an adjuvant therapy to delay and reduce the need for anti-VEGF therapy in nAMD patients.

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Investigation of lncRNA expression profiles and analysis of immune-related lncRNA-miRNA-mRNA networks in neovascular age-related macular degeneration

Project description:The aim of the present study was to investigate the alteration of lncRNAs and mRNAs in neovascular AMD. The differentially expressed mRNAs (DEmRNAs) and lncRNAs (DElncRNAs) were identified and the immune-related ceRNA network was characterized.

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

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Macrophage elastase (MMP12) critically contributes to the development of subretinal fibrosis

Project description:Macular subretinal fibrosis is the end-stage complication of neovascular age-related macular degeneration (nAMD). RPE/Choroid from control and subretinal fibrosis mice were collected and processed for RNA sequencing (RNA-seq) analysis to investigate the molecular mechanism of subretinal fibrosis.

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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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