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Single-Cell Multiomics Profiling Reveals Heterogeneity of Müller Cells in the Oxygen-Induced Retinopathy Model

ABSTRACT: Single-Cell Multiomics Profiling Reveals Heterogeneity of Müller Cells in the Oxygen-Induced Retinopathy Model

PROVIDER: PRJNA1193014 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31567344_1.fastq.gz	Fastqsanger.gz
	SRR31567344_2.fastq.gz	Fastqsanger.gz
	SRR31567345_1.fastq.gz	Fastqsanger.gz
	SRR31567345_2.fastq.gz	Fastqsanger.gz

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Single-Cell Multiomics Profiling Reveals Heterogeneity of Müller Cells in the Oxygen-Induced Retinopathy Model

Project description:Retinal neovascularization poses heightened risks of vision loss and blindness. Despite its clinical significance, the molecular mechanisms underlying the pathogenesis of retinal neovascularization remain elusive. This study utilized single-cell multiomics profiling in an oxygen-induced retinopathy (OIR) model to comprehensively investigate the intricate molecular landscape of retinal neovascularization.

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Single-cell RNA sequencing reveals that Epac1 deletion attenuates Müller glial pathological activation in ischemia-induced retinopathy

Project description:Here we report the single-cell RNA sequencing (scRNA-seq) analysis of retinas from WT and Epac1-knockout mice under Oxygen-Induced Retinopathy (OIR) and Room Air (RA) conditions. The OIR model was induced by exposing pups to 70% oxygen from postnatal day 7 (P7) to P12. This study aims to delineate the cellular heterogeneity and investigate the neuroprotective mechanisms associated with Epac1 deletion, with a specific focus on Müller glial pathological activation and retinal neurodegeneration. Retinal tissues were collected at postnatal day 17 (P17) to establish a comprehensive transcriptomic profile of the ischemia-induced retinopathy model.

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RiboTag-based profiling of actively translating transcripts in Nrf2-deficient and wildtype Müller cells in a mouse model of oxygen-induced retinopathy

Project description:Müller cells play a critical role in retinal angiogenesis and inflammation, particularly in ischemic retinopathies such as oxygen-induced retinopathy (OIR). Here, we employed actively translating transcriptome profiling using RiboTag technology to selectively examine gene expression in Müller cells with and without Nrf2, a master regulator of oxidative stress responses, during OIR. Conditional deletion of Nrf2 in Müller cells exacerbated retinal avascular areas and pathological neovascularization in the OIR model, without altering Müller cell number or viability. RiboTag-based RNA sequencing and pathway analysis identified dysregulation of oxidative phosphorylation and acute phase signaling, along with suppression of pathways related to neuronal signaling. Müller cell Nrf2 deficiency resulted in dysregulation of multiple genes involved in acute-phase response, inflammation, and angiogenesis. These findings uncover a critical role for Nrf2 in maintaining Müller cell homeostasis and identify molecular signatures by which its loss amplifies retinal gliosis and pathological angiogenesis.

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Effects of inhibitors in mice with oxygen-induced retinopathy

Project description:Analysis of gene expression changes in oxygen-induced retinopathy mice treated intravitreally with inhibitors. oxygen-induced retinopathy(OIR)mice is one of the experimental systems that mimic retinal ischemic diseases. This model is widely used as an evaluation system for various surgical procedures.

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Hyperoxia induces glutamine-fuelled anaplerosis in retinal Müller cells

Project description:Premature infants require oxygen supplementation to survive, but excess oxygen causes retinovascular growth suppression that underlies the leading cause of infant blindness known as retinopathy of prematurity (ROP). We analyzed changes in intermediary metabolism during hyperoxia in human retinal endothelial cells (RECs) and human retinal Müller glia, which coexist through glutamine consumption and production, respectively. Using a stable isotope labeling technique in human RECs and human Müller cells in culture, here we show that Müller cells in hyperoxia block entry of glycolytic carbon into the tricarboxylic acid (TCA) cycle and instead oxidize glutamine. In hyperoxia, catabolism of glutamine increased ammonium release by 2-fold. Hyperoxia induces glutamine-fueled anaplerosis that reverses basal Müller cell metabolism from production to consumption of glutamine.

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C57Bl6J retina lysates in oxygen-induced retinopathy

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microRNA expression profile in retina and choroid in oxygen-induced retinopathy model

Project description:Using Next Generation Sequencing (NGS) we profiled miRNA expression in the retina and choroid during degenerative and NV phases of oxygen-induced retinopathy (OIR).

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