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Overlapping transcriptional programs promote survival and axonal regeneration of injured retinal ganglion cells [1]

ABSTRACT: Overlapping transcriptional programs promote survival and axonal regeneration of injured retinal ganglion cells [1]

PROVIDER: PRJNA830507 | ENA |

REPOSITORIES: ENA

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Overlapping transcriptional programs promote survival and axonal regeneration of injured retinal ganglion cells

Project description:Overlapping transcriptional programs promote survival and axonal regeneration of injured retinal ganglion cells

| PRJNA834803 | ENA

Overlapping transcriptional programs promote survival and axonal regeneration of injured retinal ganglion cells [2]

Project description:Overlapping transcriptional programs promote survival and axonal regeneration of injured retinal ganglion cells [2]

| PRJNA834807 | ENA

Overlapping transcriptional programs promote survival and axonal regeneration of injured retinal ganglion cells [1]

Project description:Neurons of the central nervous system (CNS) display only a limited ability to survive and regenerate their axons after an injury. In mice, 85% of retinal ganglion cells (RGCs) die within 2 weeks of axotomy by optic nerve crush (ONC) and only few survivors regenerate axons. In the past years, a multitude of interventions have been identified to improve RGC survival and regeneration after an injury, however, each only protects a subset of neurons and stimulates axon regrowth in an even smaller set.. Here, we sought out to elucidate the molecular mechanisms underlying this selective responsiveness and investigated genes regulated by three well established survival and regeneration-promoting interventions – activation of the MTOR pathway via deletion of its inhibitor Pten, activation of the Jak/Stat-pathway by deletion of its endogenous inhibitor Socs3, and overexpression of the neurotrophic cytokine CNTF. Analysis of the transcriptomes from >125,000 single RGCs at various time points after ONC showed that while broad survival of all RGC types could be induced with each intervention, type-independent axon regeneration was only overcome with the manipulation of multiple pathways. Those RGCs were able to mitigate the injury response and simultaneously upregulated survival and regeneration associated programs (prior and after injury). Four independent ways of analysis identified these programs to be differentially regulated among RGCs, with distinct signatures for degenerating, surviving and regenerating cells. Finally, testing some genes associated with the regeneration-program in vivo identified potential future therapeutic targets to promote neuroprotection and axonal regeneration.

2022-06-28 | GSE201254 | GEO

Overlapping transcriptional programs promote survival and axonal regeneration of injured retinal ganglion cells [2]

2022-06-28 | GSE202154 | GEO

Overlapping transcriptional programs promote survival and axonal regeneration of injured retinal ganglion cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-06-28 | GSE202155 | GEO

Amacrine cells suppress retinal ganglion cells survival and optic nerve regeneration bu releasing intersynaptic zinc

Project description:Retinal ganglion cells (RGCs) convey the major output of information collected from the eye to the brain. RGCs are irreversibly lost when injured in degenerative diseases such as glaucoma; this failure can be partially reversed by eliminating the retinal mobile zinc (Zn2+) and leads to substantial axon regeneration. ZnT3 conditional knockout in retinal amacrine cells blocks the synaptic transport of Zn2+, which promotes RGC survival and axonal regeneration in optic nerve jinjury (ONC). Here, we conducted an mRNA sequencing of flow cytometry-isolated RGCs 3 days after optic nerve injury with or without ZnT3 expression in retinal amacrine cells.

2023-07-01 | GSE213937 | GEO

Transcriptional control of retinal ganglion cell death after axonal injury

Project description:Transcriptional control of retinal ganglion cell death after axonal injury

| PRJNA713995 | ENA

Chromatin accessibility and transcriptome changes in injured retinal ganglion cells (RGCs) after Arid1a deletion

Project description:To gain a deeper insight into roles of Arid1a in injured retinal ganglion cells (RGCs), we performed ATAC-seq and RNA-seq to analyze the genome-wide changes of chromatin accessibility and transcriptome changes before and after Arid1a deletion in RGCs of the adult mouse using Cre-lox system.

2020-04-20 | GSE147844 | GEO

Global transcriptome analysis reveals differences between embryonic and adult dorsal root ganglion axonal mRNAs that are implicated in axonal growth and pain

Project description:Local protein synthesis in sensory neuron axons is necessary for axonal regeneration with the efficiency of regeneration decreasing with age. Because the full repertoire of transcripts in embryonic and adult rat sensory axons is unknown we asked how the pool of mRNAs dynamically changes during ageing. We isolated mRNA from pure axons and growth cones devoid of non-neuronal or cell body contamination. Genome-wide microarray analysis reveals that a previously unappreciated number of transcripts are localised in sensory axons and that this repertoire changes during development toward adulthood. Embryonic sensory axons are enriched in transcripts encoding cytoskeletal-related proteins with a role in axonal outgrowth. Surprisingly, adult axons are highly enriched in mRNAs encoding immune molecules with a role in nociception. To validate our experimental approach we show that Tubulin-beta3 mRNA is present only in embryonic axons where it is locally synthesised. In summary, we show that the population of axonal mRNAs dynamically changes during development, which may partly contribute to the intrinsic capacity of axons at different ages to regenerate after injury and to modulate pain. Pure axonal RNA were extracted from the axons of embryonic and adult dorsal root ganglion neurons, each with 5 biological replicates. The axonal transcriptomes were analysed using Affymetrix Rat Genome 230 2.0 Arrays.

2010-11-23 | E-GEOD-22638 | biostudies-arrayexpress

Robust axonal regeneration occurs in the injured CAST/Ei mouse central nervous system

Project description:Axon regeneration in the central nervous system (CNS) requires reactivating injured neurons’ intrinsic growth state and enabling growth in an inhibitory environment. Using an inbred mouse neuronal phenotypic screen, we find that CAST/Ei mouse adult dorsal root ganglion neurons extend axons more on CNS myelin than the other eight strains tested, especially when pre-injured. Injury-primed CAST/Ei neurons also regenerate markedly in the spinal cord and optic nerve more than those from C57BL/6 mice and show greater spouting following ischemic stroke. Heritability estimates indicate that extended growth in CAST/Ei neurons on myelin is genetically determined, and two whole-genome expression screens yield the Activin transcript Inhba as most correlated with this ability. These screens are presented here. Biological quadruplicate - Mouse tissue - Naïve Dorsal Root Ganglia (DRG) and 5 day post sciatic nerve crush DRG - x9 strains.

2015-07-22 | E-GEOD-67130 | biostudies-arrayexpress

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