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METTL14 promotes retinal neovascularization via m6A-modification on MXD1 mRNA in oxygen induced retinopathy

ABSTRACT: In this study, we explored the effects and underlying mechanisms of methyltransferase-like 14 (METTL14) in microglia cell line (HMC3 cells), which are crucial for the pathogenesis of Retinopathy of Prematurity (ROP). Our results showed that the expression of METTL14 was increased in HMC3 cells after hypoxia stimulation. MeRIP-seq and RNA-seq were performed to explore the underlying mechanisms.

ORGANISM(S): Homo sapiens

PROVIDER: GSE267797 | GEO | 2025/06/30

REPOSITORIES: GEO

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Circular RNA Profiling in Peripheral Blood Mononuclear Cells from Retinopathy of Prematurity

Project description:To reveal the altered expression profiles of circular RNAs (circRNAs) in the peripheral blood mononuclear cells (PBMCs) of patients with retinopathy of prematurity (ROP), microarray analysis was conducted in the samples from ROP patients and controls.

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Chronic intermittent hypoxia inhibits the revascularization of the ischemic retina and aggravates neurodegeneration and neovascularization

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Timed topical dexamethasone eye drops improve mitochondrial function to suppress severe retinopathy of prematurity.

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METTL14 promotes retinal neovascularization via m6A-modification on MXD1 mRNA in oxygen induced retinopathy

Project description:METTL14 promotes retinal neovascularization via m6A-modification on MXD1 mRNA in oxygen induced retinopathy

| PRJNA1112889 | ENA

Epithelial membrane protein-2 promotes VEGF signaling to promote pathological neovascular growth in retinopathy of prematurity

Project description:Retinopathy of prematurity (ROP) is a leading cause of childhood blindness, and exclusively affects infants born prematurely. In this study, we test the hypothesis that EMP2 contributes to neovascularization in a mouse model of the disease. We show that EMP2 promotes neuronal VEGF signaling and that its downregulation reduces severity of neovascularization.

2021-12-17 | GSE123945 | GEO

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2021-02-22 | GSE158799 | GEO

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Project description:Oxygen-induced retinopathy (OIR) animal model is widely used for retinopathy of prematurity (ROP). The purpose of this project was to identify proteins and related pathways of OIR with or without anti-vascular endothelial growth factor (VEGF) treatment, for use as biomarkers in diagnosing and treating ROP.

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Placental Inflammation Significantly Correlates with Reduced Risk for Retinopathy of Prematurity

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Project description:Retinopathy of prematurity (ROP) is a disorder of the developing retina of preterm infants. ROP can lead to blindness due to abnormal angiogenesis that is the result of suspended vascular development and vaso-obliteration leading to severe retinal stress and hypoxia. We tested the hypothesis that a combined treatment with two human progenitor populations, the CD34+ cells, bone marrow-derived, and the endothelial colony-forming cells (ECFCs) synergistically protected the developing retinal vasculature in a murine model of ROP, the oxygen-induced retinopathy (OIR)., CD34+ cells alone, ECFCs alone, or a combination thereof were injected intravitreally at either P5 or P12 and pups were euthanized at P17. Retinas from OIR mice injected with ECFCs or the combined treatment revealed formation of the deep vascular plexus (DVP) while still in hyperoxia, with normal appearing connections between the superficial vascular plexus (SVP) and the DVP. The combination therapy prevented aberrant retinal neovascularization and was more effective anatomically and functionally at rescuing the ischemia phenotype than either cell type alone. The beneficial effect of the cell combination was the result of their ability to orchestrate an acceleration of vascular development and more rapid ensheathment of pericytes on the developing vessels.

2019-12-31 | GSE135844 | GEO

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