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

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

PROVIDER: PRJNA510363 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8329440.fastq.gz	Fastqsanger.gz
	SRR8329441.fastq.gz	Fastqsanger.gz
	SRR8329442.fastq.gz	Fastqsanger.gz
	SRR8329443.fastq.gz	Fastqsanger.gz
	SRR8329434.fastq.gz	Fastqsanger.gz

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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

4D label-free proteomics analysis of oxygen-induced retinopathy with or without anti-VEGF treatment

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.

2023-09-14 | PXD045378 |

RNA-Seq Provides Insights into VEGF-Induced Signaling in Human Retinal Microvascular Endothelial Cells: Implications in Retinopathy of Prematurity [RNA-seq_2]

Project description:The pathophysiology of retinopathy of prematurity (ROP) is postulated to first involve delayed intraretinal vascularization, followed by intravitreal neovascularization (IVNV). Although intravitreal agents that reduce the bioactivity of vascular endothelial growth factor (VEGF) are used to treat IVNV, concerns exist regarding their effects on intraretinal vascularization. In an experimental ROP model, VEGF receptor 2 (VEGFR2) knockdown in retinal endothelial cells reduced IVNV and promoted intraretinal vascularization, whereas knockdown of a downstream effector, signal transducer and activator of transcription 3 (STAT3) in retinal endothelial cells only reduced IVNV. In this study, we tested the hypothesis that the different pathways involved in VEGF-triggered VEGFR2 signaling and VEGF-triggered STAT3 signaling in retinal endothelial cells would allow us to delineate signaling pathways involved in IVNV from those involved in intraretinal vascularization in ROP. To address our hypothesis, we used RNA-sequencing and pathway enrichment analysis to determine changes in the transcriptome of cultured human retinal microvascular endothelial cells (HRMECs). Of the enriched pathways, inactivation of oncostatin M signaling was predicted by either KDR or STAT3 knockdown in the presence of VEGF. Activation of kinetochore metaphase signaling was predicted by KDR knockdown, whereas inactivation was predicted by STAT3 knockdown in the presence of VEGF. Inactivation of signaling by the Rho family of GTPases was predicted by KDR knockdown, but activation was predicted by STAT3 knockdown in the presence of VEGF. Taken together, our data identified unique signaling pathway differences between VEGF-triggered VEGFR2 and VEGF-triggered STAT3 in HRMECs that might have implications in ROP.

2022-12-29 | GSE221861 | GEO

RNA-Seq Provides Insights into VEGF-Induced Signaling in Human Retinal Microvascular Endothelial Cells: Implications in Retinopathy of Prematurity [RNA-seq_1]

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RNA-sequencing of the oxygen induced retinopathy (OIR) model in C57BL/6 mice

Project description:Pathological retinal angiogenesis is one of the major causes of vision loss worldwide. The breakdown of blood vessels and aberrant vessels growth usually lead to hemorrhage, macular edema, fibrotic scar, and retinal detachment. OIR model serves as a proxy for human pathological retinal neovascularization such as proliferative diabetic retinopathy, retinal vein occlusion and retinopathy of prematurity. C57BL/6 mice were exposed to 75% O2 in a hyperoxic chamber from postnatal day P7 to P12 and then returned to room air. The greatest neovascular response occurred at postnatal 17 days (P17) when the mice are put back to room air condition for 5 days. In order to reveal potential genes that involve in pathological neovascularization, we performed transcriptomic analyses of retina of P17.

2024-08-20 | GSE241239 | GEO

C57Bl6J retina lysates in oxygen-induced retinopathy

Project description:Schemic retinopathies such as diabetic retinopathy (DR) and retinopathy of prematurity (ROP), are the main causes of blindness in working age and pediatric populations in industrialized countries. It is estimated that close to 100 million individuals worldwide suffer from DR and 15 million preterm infants born each year are predisposed to ROP. Regrettably, relatively little is known of the cellular processes at play during late stages of pathological angiogenesis in these diseases and consequently current standards of care target all neovascularization. Oxygen-induced retinopathy (OIR) allows to reproduce experimentally in the mouse retina the pathological features observed in human pathological retina such as ischemic avascular regions as well as epi-retinal neovascularization. Using agnostic and orthogonal approaches, in our work we demonstrate that in contrast to healthy blood vessels, pathological vessels engage pathways of cell cycle arrest, resulting in cellular senescence. These findings combined with further genetic and pharmacological approaches provide mechanistic evidence supporting that targeting selectively senescent vessels in DR represents a potential treatment for neovascular retinal disease.

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

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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

Clinical and Genetic Analysis of Retinopathy of Prematurity-GWAS

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Project description:Clinical and Genetic Analysis of Retinopathy of Prematurity-GWAS

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