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Optic nerve crush induces spatial and temporal gene expression patterns in retina of BALB/cJ mice

ABSTRACT: Central nervous system (CNS) trauma and neurodegenerative disorders trigger a cascade of cellular and molecular events resulting in neuronal apoptosis and regenerative failure. The pathogenic mechanisms and gene expression changes associated with these detrimental events can be effectively studied using a rodent optic nerve crush (ONC) model. The purpose of this study was to use a mouse ONC model to: (a) evaluate changes in retina gene expression, (b) identify neurodegenerative pathogenic pathways and (c) discover potential new therapeutic targets. Affymetrix Mouse Gene 1.0 ST arrays were utlized to detail the global gene expression profile following optic nerve crush (ONC) in the retina of BALB/cJ mice at six different days post crush (dpc) (naive, 3 dpc, 7 dpc, 14 dpc, 21 dpc and 28 dpc) to understand the pathogenic responses in relation to neuronal loss and regenerative failure.

ORGANISM(S): Mus musculus

PROVIDER: GSE44707 | GEO | 2014/06/17

SECONDARY ACCESSION(S): PRJNA191065

REPOSITORIES: GEO

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Optic nerve crush induces spatial and temporal gene expression patterns in optic nerve of BALB/cJ mice

Project description:Central nervous system (CNS) trauma and neurodegenerative disorders trigger a cascade of cellular and molecular events resulting in neuronal apoptosis and regenerative failure. The pathogenic mechanisms and gene expression changes associated with these detrimental events can be effectively studied using a rodent optic nerve crush (ONC) model. The purpose of this study was to use a mouse ONC model to: (a) evaluate changes in optic nerve (ON) gene expression, (b) identify neurodegenerative pathogenic pathways and (c) discover potential new therapeutic targets. Affymetrix Mouse Gene 1.0 ST arrays were utlized to detail the global gene expression profile following optic nerve crush (ONC) in the ON of BALB/cJ mice at six different days post crush (dpc) (naive, 3 dpc, 7 dpc, 14 dpc, 21 dpc and 28 dpc) to understand the pathogenic responses in relation to neuronal loss and regenerative failure.

2014-06-17 | GSE44705 | GEO

Integrated analyses of zebrafish miRNA and mRNA expression profiles identify miR-29b and miR-223 as potential regulators of optic nerve regeneration

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Quantitative Proteomic Analysis of C57BL/6J mice after optic nerve crush Using iTRAQ Labeling

Project description:We used two groups of C57BL/6J mice, one with optic nerve crush on one eye, and another with no crush as control. Three mice were subjected to optic nerve crush, with sample names 121, 113, 114 and two were used as control with sample names 118 and 119. For the optic nerve crush, a surgical peritomy was made behind and above the eyeball and the eye muscles were gently retracted to expose the optic nerve. Dumont #5 forceps (FST) were used to crush the optic nerve approximately 0.5-1 mm behind the globe without damaging retinal vessels or affecting the blood supply.

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Dlk response to optic nerve injury

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Intercellular communication atlas reveals Oprm1 as a neuroprotective factor for retinal ganglion cells

Project description:The neuronal cell death results in neurodegenerative diseases. The extracellular environment plays a critical role in regulating cell viability. In this study, we explore how intercellular communication contributes to the survival of retinal ganglion cells (RGCs) following the optic nerve crush (ONC). By performing single-cell RNA-seq on whole retinal cells, we observed transcriptomic responses in non-RGC retinal cells to the injury, with astrocytes and Müller glia having the most interactions with RGCs. By comparing the RGC subclasses showing distinct resilience cell death, we identified top 47 interactions that are stronger in the high-survival RGCs, likely representing neuroprotective interactions. We performed functional assays on one of the receptors, Mu-opioid receptor (Oprm1). Although Oprm1 is preferentially expressed in intrinsically photosensitive retinal ganglion cells (ipRGCs), its neuroprotective effect could be transferred to multiple RGC subclasses by specific overexpressing Oprm1 in pan-RGCs. Our study provides an atlas of cell-cell interactions in both intact and post-ONC retina and an effective strategy to predict molecular mechanisms in neuroprotection, underlying the principal role played by extracellular environment in supporting neuron survival.

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Project description:Neuronal types in the central nervous system differ dramatically in their resilience to injury or insults. Here we studied selective resilience in mouse retinal ganglion cells (RGCs) following optic nerve crush (ONC), which severs their axons and leads to death of ~80% of RGCs in 2 weeks. To identify expression programs associated with differential resilience, we first used single-cell RNA-seq (scRNA-seq) to generate a comprehensive molecular atlas of 45 RGC types in adult retina. We tracked their survival after ONC, characterized transcriptomic, morphological, and physiological changes that preceded degeneration, and identified genes selectively expressed by each type. Finally, loss- and gain-of-function assays in vivo showed that manipulating some of these genes improved neuronal survival and axon regeneration following ONC. This study provides a systematic framework for parsing type-specific responses to injury, and demonstrates that these responses can be used to reveal molecular targets for intervention.

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