Electrical stimulation accelerate Wallerian degeneration and promote peripheral nerve regeneration.
Ontology highlight
ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE220261 | GEO | 2023/05/01
REPOSITORIES: GEO
Similar Datasets
Project description:Wallerian degeneration (WD) involves the fragmentation of axonal segments disconnected from their cell bodies, segmentation of the myelin sheath, and removal of debris by Schwann cells and immune cells. The removal and downregulation of myelin-associated inhibitors of axonal regeneration and synthesis of growth factors by these two cell types are critical responses to successful nerve repair. Here, we analyzed the transcriptome of the sciatic nerve of mice carrying the Wallerian degeneration slow (WldS) mutant gene, a gene that confers axonal protection in the distal stump after injury, therefore causing significant delays in WD, neuroinflammation, and axonal regeneration.
2011-06-01 | GSE22291 | GEO
Project description:Wallerian degeneration (WD) involves the fragmentation of axonal segments disconnected from their cell bodies, segmentation of the myelin sheath, and removal of debris by Schwann cells and immune cells. The removal and downregulation of myelin-associated inhibitors of axonal regeneration and synthesis of growth factors by these two cell types are critical responses to successful nerve repair. Here, we analyzed the transcriptome of the sciatic nerve of mice carrying the Wallerian degeneration slow (WldS) mutant gene, a gene that confers axonal protection in the distal stump after injury, therefore causing significant delays in WD, neuroinflammation, and axonal regeneration. 56 C57BL6 mice and 56 C57BL/6 OlaHsd-Wlds mice were anesthetized with isoflurane and underwent a microcrush lesion of their left sciatic nerve at the mid-thigh level (exept naive mice, t0). At 0, 3, 7 and 14 days post-injury, mice were anesthetized and killed by cervical dislocation. Sciatic nerves were collected and conective tissue removed. A 4-mm long sciatic nerve segment was taken from the nerve distal stump, starting at 1 mm distal from the lesion up to 5 mm distal. Distal nerve stumps were pooled by group and RNA extracted. Samples were hybridized to GeneChip® Mouse Genome 430 2.0 Array (Affymetrix). Biological replicate was done.
2011-06-01 | E-GEOD-22291 | biostudies-arrayexpress
Project description:Imaging resident and recruited macrophage contributions to Wallerian degeneration
| PRJNA638627 | ENA
Project description:Analysis of the effect of electrical field stimulation frequency at the gene expression level. Electrical stimulation has been shown to mature nascent cardiomyocytes and alter their beating properties. The purpose of the array was to identify potential mediators of these effects. Total RNA was isolated from cardiomyocytes subjected to 0.5 Hz, 1 Hz, or 2 Hz continuous electrical stimulation for 7 days, compared to an unstimulated control. Three samples from each group were analyzed
2015-11-05 | E-GEOD-74669 | biostudies-arrayexpress
Project description:Interventions: Group TEAS:percutaneous acupoint nerve electrical stimulation;Group CON:nothing
Primary outcome(s): MMSE, Mini-mental State Examination;QoR-40, 40-Item Quality of Restoration;cortisol;noradrenaline;D-LAC;DAO
Study Design: Parallel
| 81648 | ecrin-mdr-crc
Project description:We looked for soluble mediators of electrical signals in A. thaliana. To identify such molecules we fractionated fresh leaf extract and assayed the activity of fractions by analyzing electrical signals induced by each fraction. Active fractions were subjected to Mass spectrometry analysis to identify proteins contained.
2023-03-06 | PXD031220 | Pride
Project description:Analysis of the effect of electrical field stimulation frequency at the gene expression level. Electrical stimulation has been shown to mature nascent cardiomyocytes and alter their beating properties. The purpose of the array was to identify potential mediators of these effects.
2015-11-05 | GSE74669 | GEO
Project description:Current standards for safe delivery of electrical stimulation to the central nervous system are based on foundational studies which examined post-mortem tissue for histological signs of damage. This set of observations and the subsequently proposed limits to safe stimulation, termed the “Shannon limits,” allow for a simple calculation (using charge per phase and charge density) to determine the intensity of electrical stimulation that can be delivered safely to brain tissue. In the three decades since the Shannon limits were reported, advances in molecular biology have allowed for more nuanced and detailed approaches to be used to expand current understanding of the physiological effects of stimulation. Here, we investigated spatial transcriptomics as a new approach to assess the safety and efficacy of electrical stimulation in the brain. Electrical stimulation was delivered to the rat visual cortex with either acute or chronic electrode implantation procedures (acute: tissue collection 3 hours post-stimulation on the day of surgery; chronic: stimulation delivered 1-month post-implantation, and tissue collection 24 hours later). To explore the influence of device type and stimulation parameters, we used carbon fiber ultramicroelectrode arrays (7 µm diameter) and microwire electrode arrays (50 µm diameter) delivering charge and charge density levels selected above and below reported tissue damage thresholds (range: 2-20 nC, 0.1-1 mC/cm2). Spatial transcriptomics was performed using Visium Spatial Gene Expression Slides (10x Genomics), which enabled simultaneous immunohistochemistry and spatial transcriptomics to directly compare traditional histological metrics to transcriptional profiles within each tissue sample. Our data revealed unique spatial patterns of differentially expressed genes that are related to cellular processes including inflammation, cell cycle progression, and plasticity. Effects were dependent on stimulation parameters and were localized to both traditional and ultra-small device locations. The abundance of data gathered using this approach allows for sophisticated analysis that can be used to generate new hypotheses while also revealing novel potential biomarkers of neurostimulation.
2022-07-01 | GSE202425 | GEO
Project description:Retinal degeneration is the leading cause of irreversible blindness. Retinitis pigmentosa (RP) is a genetically heterogenous group of diseases. In the United States, approximately one in 4000 individuals is affected. RP begins with the loss of night vision due to the loss of rod photoreceptor cells. The disease progresses slowly with the loss of peripheral vision, and eventually leads to complete debilitating and irreversible blindness. The first mutation associated with human RP was identified in the gene encoding rhodopsin, the G-protein coupled receptor of rod photoreceptor cells. Mutations within the rhodopsin gene account for significant portion of RP cases. Specifically, mutations of the proline at residue 347 in rhodopsin have been linked to human RP. We are fortunate to have access to the P347S rhodopsin mutant mice. These mice represent an excellent transgenic mouse model of retinal degeneration. The P347S rhodopsin mutation is one of the best studied mutations, yet the mechanism by which the mutation causes degeneration is still unknown. One study has demonstrated that galectin-1 plays a role in degeneration of neuronal processes (1) and another study has shown that expression level of galectin-3 is elevated in retinas of patients with age-related macular degeneration. These studies in conjunction with the availibility of the P347S mutant mice have provided impetus to examine the pathogenesis of retinal degeneration in the context of the possible role of glycans and glycan-binding proteins. The time course of photoreceptor degeneration in the P347S mouse model has been carefully studied. In these mice, degeneration is barely detectable at 1 month of age, yet biochemical evidence suggests that the rod photoreceptor cells have already begun to die. At 4 months of age, approximately half of the rod photoreceptor cells have degenerated. To distinguish involvement of glycogens at the various stages of retinal degeneration, we have collected retinas of wild type and the mutant mice at four time points (1, 2, 3, and 4 months of age). This will allow us to identify the genes that target early, mid- and late stages of the retinal degeneration process. Thus we request the analysis of total 24 samples as specified below: Age Group (months) Mice No of samples at each time point 1 Wild type 3 2 Wild type 3 3 Wild type 3 4 Wild type 3 1 P347S 3 2 P347S 3 3 P347S 3 4 P347S 3 Total 24.
2011-09-07 | E-GEOD-31990 | biostudies-arrayexpress
Project description:Human primary myotubes +/- electrical pulse stimulation
| PRJEB46916 | ENA