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Sciatic nerve crush regulation of RNA alternative poly-adenylation

ABSTRACT: Sciatic nerve crush regulation of RNA alternative poly-adenylation

PROVIDER: PRJNA962456 | ENA |

REPOSITORIES: ENA

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Sciatic nerve crush regulation of RNA alternative poly-adenylation [DRGinjury_2019-QuantSeq_Rev_24h]

Project description:Sciatic nerve crush regulation of RNA alternative poly-adenylation [DRGinjury_2019-QuantSeq_Rev_24h]

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Gene expression from aged and young sciatic nerve after nerve injury

Project description:Sciatic nerve ligation was performed on cohorts of 2-month and 24-month old animals. Resulting gene-expression data were generated from sciatic nerve 1 and 4 days after injury compared to naïve animals. Results show differences in sciatic nerve responses with normal aging. Total RNA taken from sciatic nerves from 2-month and 24-month old animals at either day 0, 1 and 4 after sciatic nerve crush injury.

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Project description:To profile downstream gene-expression changes regulated by DLK, we profiled motoneurons in the lumbar spinal cord using RiboTag, following sciatic nerve crush in both control and Dlk conditional knockout (Dlk ΔMN) mice. We found that DLK regulates the expression of many secreted proteins, which have the potential to influence the behavior of other cells, including the immune system.

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DLK-gated responses in motoneurons following sciatic nerve crush

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Skeletal muscle transcriptomics identifies common pathways in nerve crush injury and ageing

Project description:Motor unit remodelling involving repeated denervation and re-innervation occurs throughout life. The efficiency of this process declines with age contributing to neuromuscular deficits. We investigated differentially expressed genes (DEG) in muscle following peroneal nerve crush to model of motor unit remodelling in C57Bl6 mice. Muscle RNA was isolated at 3 days post-crush, RNA libraries were generated using poly-A selection, sequenced.

2022-01-10 | E-MTAB-10601 | biostudies-arrayexpress

Expression data from mouse optic nerve head after optic nerve crush

Project description:Reactive gliosis is a complex process that involves profound changes in gene expression. We used microarray to indentify differentially expressed genes and to investigate the molecular mechanisms of reactive gliosis in optic nerve head in response to optic nerve crush injury. C57Bl/6 female mice were 6-8 weeks old at the time of optic nerve crush surgery. The optic nerve in the left eye was crush 1 mm behind the globe for 10 seconds and the right eye served as contralateral control. The animals were allowed to recover for 1 day, 3 day, 1 week, 3 weeks and 3 months before the optic nerve heads were collected. The naive control mice did not receive any surgery in either eye. Due to the small tissue size of the mouse optic nerve head, two optic nerve heads were pooled together for each microarray chip. The left eyes and the right eyes of two mice were combined respectively to form one pair of experiment and control samples. There were five biological replicates (10 mice) for each condition.

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Sciatic nerve crush upregulation of B2-SINE expression at specific genomic loci

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Single Cell Atlas of Injured Sciatic Nerve Tissue

Project description:Sciatic nerve crush (SNC) triggers sterile inflammation within the distal nerve and de-afferented dorsal root ganglia (DRGs). In the nerve, neutrophils and pro-inflammatory Ly6Chigh monocytes appear first and rapidly give way to Ly6Clow resolving macrophages. Transcriptional profiling of injured nerve tissue identifies six macrophage subpopulations, repair Schwann cells and mesenchymal cells as the main cell types. Macrophages at the nerve crush site are distinct from macrophages associated with degenerating nerve fibers. Monocytes and macrophages in the injured nerve “eat” apoptotic cell corpses of leukocytes and thereby contribute to an anti-inflammatory milieu. Studies with chimeric mice show that following SNC few blood-derived immune cells enter DRGs. Myeloid cells in the injured nerve, but not DRGs, express the receptor for the chemokine GM-CSF. In the absence of GM-CSF, conditioning-lesion induced regeneration of DRG neuron central projections is abrogated. Thus, a carefully orchestrated immune response in the nerve is required for conditioning-lesion induced neurorepair.

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