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HDAC3 ChIP sequencing of L4-L6 Dorsal Root Ganglia upon spinal or sciatic axonal injury

ABSTRACT: Purpose: A) compare the response to an axonal injury in the peripheral vs central nervous system B) clarify the role of HDAC3 in axonal regeneration Results: we found that after peripheral axonal injury there is a higher number of differentially expressed genes regulated by HDAC3 with respect to central injury with a number of genes associated with regenerative pathways

ORGANISM(S): Mus musculus

PROVIDER: GSE104977 | GEO | 2018/10/01

REPOSITORIES: GEO

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H3K9ac, H3K27ac, H3K27me3 ChIP sequencing and ATAC sequencing of L4-L6 Dorsal Root Ganglia upon spinal or sciatic axonal injury

Project description:Purpose: compare the epigenetic response of DRG neurons to an axonal injury in the peripheral vs central nervous system by measuring accessible chromatin and several histone marks Results: we found that after peripheral axonal injury there is a much greater number of epigenetic changes than after central spinal injury, and that these epigenetic changes after peripheral axotomy tended toward increased chromatin accessibility.

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HDAC3 ChIP sequencing of L4-L6 Dorsal Root Ganglia upon spinal or sciatic axonal injury

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RNA sequencing of Dorsal Root Ganglia upon axonal injury, in presence or absence of NAC (N-acetyl cysteine), and upon H2O2 nerve treatment

Project description:Purpose: A) compare the response to an axonal injury in the peripheral vs central nervous system B) clarify the mechanism of Reactive Oxygen Species-dependent axonal regeneration Results: we found that after peripheral axonal injury there is a higher number of differentially expressed genes with respect to central injury. Moreover,inflammation related genes and regeneration-associated genes were differentially regulated after peripheral injury and H2O2, but less after central injury. Signalling pathways and biological processes related to injury-dependent nerve regeneration were reduced with the addition of NAC at the time of sciatic injury compared to vehicle.

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ATAC sequencing and RNA sequencing of L4-L6 mouse Dorsal Root Ganglia upon dorsal column axotomy plus injection of the histone deacetylase inhibitor MS275

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H3K9ac, H3K27ac, H3K27me3 ChIP sequencing and ATAC sequencing of L4-L6 Dorsal Root Ganglia upon spinal or sciatic axonal injury

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scRNAseq analysis of mouse L4 whole dorsal root ganglions following sciatic nerve cush, dorsal root crush and spinal cord injury

Project description:After an injury in the adult mammalian central nervous system, lesioned axons fail to regenerate. This failure to regenerate contrasts with the remarkable potential of axons to grow following an injury in the peripheral nervous system. Peripheral sensory neurons with cell soma in dorsal root ganglia (DRG) switch to a regenerative state after nerve injury to enable axon regeneration and functional recovery. Decades of research have focused on the signaling pathways elicited by injury in sensory neurons and in Schwann cells that insulate axons as central mechanisms regulating nerve repair. However, neuronal microenvironment is far more complex and is composed of multiple cell types including endothelial, immune and glial cells. Whether the microenvironment surrounding neuronal soma contribute to the poor regenerative outcomes following central injuries remains largely unexplored. To answer this question, we performed a single cell transcriptional profiling of the DRG neuronal microenvironment response to peripheral and central injuries. In dissecting the roles of the microenvironment contribution, we have focused on a poorly studied glia population of Satellite Glial Cells (SGC) surrounding the neuronal cell soma. Upon a peripheral injury, SGC contribute to axon regeneration via Fatty acid synthase (Fasn)-PPARα signaling pathway. Our analysis reveals that in response to central injuries, SGC do not activate the PPAR signaling pathway. However, induction of this pathway with fenofibrate, an FDA- approved PPARα agonist used for dyslipidemia treatment, rescued axon regeneration following an injury to the central nerves. Collectively, our results uncovered a previously unappreciated role of the neuronal microenvironment differential response in central and peripheral injuries.

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RNA sequencing of L4-L6 mouse Dorsal Root Ganglia 3 days post sciatic nerve crush and naive following 10 days of Indole-3-propionic acid treatment

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RNA sequencing of whole sciatic Dorsal Root Ganglia (DRG) from young and aged mice

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Transcriptional reprogramming of distinct peripheral sensory neuron subtypes after axonal injury

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RNA sequence reveals mouse retinal transcriptome changes early after axonal injury

Project description:Purpose: The purpose of this study was　to use RNA-seq to investigate the molecular mechanisms of damage in the early stages of the response to axonal injury, before the onset of RGC death. Methods: 12-week-old wild-type (WT) mice were used in this study. The experiment group underwent an optic nerve crush (ONC) procedure to induce axonal injury in the right eye, and the control group underwent a sham procedure. Retinal mRNA profiles were generated by deep sequencing, in triplicate, using IlluminaHiseq2000. The sequence reads were analyzed by CLC genomics workbench and R software. qRT–PCR validation was performed using TaqMan assays. Results: Using an optimized data analysis workflow, we mapped about 66 million sequence reads per sample to the mouse genome (build mm9). Differential gene expression analysis showed that endoplasmic reticulum stress-related genes and antioxidative response-related genes have been shown to be significantly upregulated 2 days after ONC. Conclusions: Our study represents the first detailed analysis of retinal transcriptomes in the early stages after axonal injury. Our results indicated that ER stress plays a key role under these conditions. Furthermore, the antioxidative defense and immune responses occurred concurrently in the early stages after axonal injury. We believe that our study will lead to a better understanding of and insight into the molecular mechanisms underlying RGC death after axonal injury. Retinal mRNA profiles of 12 week-old wild type (WT) after ONC or sham were generated by deep sequencing, in triplicate, using Illumina Hiseq2000.

2014-02-21 | E-GEOD-55228 | biostudies-arrayexpress

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