Transcriptional change of the lesion site margins after spinal cord injury in canine
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PROVIDER: PRJNA1136153 | ENA |
REPOSITORIES: ENA
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Project description:We conduct complete SCI to canine and transplant stem cell into the lesion, in order to observe the transcriptional change of the lesion site margins,we isolate the margin tissue and performing high-throughput sequencing
2025-01-22 | GSE272307 | GEO
Project description:The goals of this study is to compare transcriptome profiles (RNA-seq) of zebrafish V2a interneurons with regrown axon and those without regrown axon in the spinal segments rostral to the lesion after spinal cord injury. For purification of V2a interneurons with regrown axon, the fluorescent tracer Rhodamine Dextran (RD) was retrogradely applied to Tg(Chx10:GFP) fish at three or eight weeks post injury. Spinal cord segments rostral to the lesion site was collected from 20 fish at 3- or 8 wpi, and corresponding spinal cord segments from 20 uninjured fish were collected as control material. GFP+/RD+ and GFP+/RD- cells were FAC-sorted and subjected to RNA-sequencing. Total RNA was isolated using SMART-SeqTM v4 UltraTM Low Input RNA Kit for Sequencing (Clontech). Sequencing libraries (N=5-6) were generated using NEBNext UltraTM RNA Library Prep Kit for Illumina following the manufacturer’s instructions (NEB). We mapped about 40-80 million sequence reads per sample to the zebrafish genome and identified 42,370 transcripts in the zebrafish V2a interneurons in the spinal cord. Our study represents the detailed analysis of transcriptomes of zebrafish V2a interneurons with regrown axon and those without regrown axon in the spinal segments rostral to the lesion after spinal cord injury.
2022-09-13 | GSE213081 | GEO
Project description:Label-free mass spectrometry-based quantitative proteomics was applied to a larval zebrafish spinal cord injury model, which allows axon regeneration and functional recovery within two days (days post lesion; dpl) after a spinal cord transection in 3 day-old larvae (dpf). Proteomic profiling of the lesion site was performed at 1 dpl and 2 dpl as well as corresponding age-matched unlesioned control tissue (4 dpf as control for 1 dpl; 5 dpf as control for 2 dpl).
2023-09-06 | PXD037590 | Pride
Project description:ContextCerebrotendinous xanthomatosis (CTX) is an autosomal recessively inherited lipid storage disease caused by mutation in the CYP27A1 gene. Spinal form CTX is a rare clinical subgroup of CTX and only 14 patients from 11 families have been reported to date. Here, we report the first Asian patient with spinal form CTX showing characteristic radiological findings.FindingsThe patient, a 46-year-old Japanese male, developed sensory disturbance of the lower legs at 39 and spastic gait at 46 years of age. Spinal cord magnetic resonance imaging (MRI) revealed a long hyperintense lesion involving lateral corticospinal tracts and gracile tracts in the cervical and thoracic cord on T2-weighted images. Gallium-67 (67Ga) scintigraphy revealed abnormal uptake in the Achilles tendons and the serum cholestanol level was elevated. CYP27A1 gene analysis identified homozygous missense mutation, c.1214G>A (p.R405Q). The patient was treated with atorvastatin monotherapy, which reduced serum cholestanol to less than 50% of the pretreatment level.ConclusionSpinal form CTX should be considered in the differential diagnosis of cryptogenic myelopathy, especially in patients with a long spinal cord lesion, as treatment with chenodeoxycholic acid and/or competitive inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase reverse the metabolic derangement and prevent the neurologiccal dysfunction.
| S-EPMC5137569 | biostudies-literature
Project description:A limited mechanistic understanding of skeletal muscle wasting after acute spinal cord injury (SCI) precludes targeted molecular interventions. Here, we demonstrate marked systemic wasting also affecting neurologically intact non-paralyzed (supralesional) muscle early after SCI. Systemic muscle mass loss propagates muscle weakness, affects fast type 2 myofibers preferentially, and becomes exacerbated after high (T3) compared to low (T9) thoracic paraplegia indicating lesion-level dependent (“neurogenic”) mechanisms. The wasting of non-paralyzed muscle, its rapid onset and severity beyond what can be explained by disuse implies additional systemic drivers. Muscle transcriptome and biochemical analysis revealed a glucocorticoid-mediated catabolic signature of SCI-induced systemic muscle wasting that was mitigated i) by endogenous glucocorticoid ablation (adrenalectomy), ii) by pharmacological glucocorticoid receptor (GR) blockade, and was iii) completely prevented, relative to T9 SCI, by genetic muscle-specific GR deletion. We provide evidence of neurogenic hypercortisolism underlying a rapid systemic and functionally relevant muscle wasting syndrome after acute SCI.
2024-01-31 | GSE224186 | GEO
Project description:AimsOlig2 is one of the most critical factors during CNS development, which belongs to b-HLH transcription factor family. Previous reports have shown that Olig2 regulates the remyelination processes in CNS demyelination diseases models. However, the role of Olig2 in contusion spinal cord injury (SCI) and the possible therapeutic effects remain obscure. This study aims to investigate the effects of overexpression Olig2 by lentivirus on adult spinal cord injury rats.MethodsLenti-Olig2 expression and control Lenti-eGFP vectors were prepared, and virus in a total of 5 μL (108 TU/mL) was locally injected into the injured spinal cord 1.5 mm rostral and caudal near the epicenter. Immunostaining, Western blot, electron microscopy, and CatWalk analyzes were employed to investigate the effects of Olig2 on spinal cord tissue repair and functional recovery.ResultsInjection of Lenti-Olig2 significantly increased the number of oligodendrocytes lineage cells and enhanced myelination after SCI. More importantly, the introduction of Olig2 greatly improved hindlimb locomotor performances. Other oligodendrocyte-related transcription factors, which were downregulated or upregulated after injury, were reversed by Olig2 induction.ConclusionsOur findings provided the evidence that overexpression Olig2 promotes myelination and locomotor recovery of contusion SCI, which gives us more understanding of Olig2 on spinal cord injury treatment.
| S-EPMC6492694 | biostudies-literature
Project description:Traumatic spinal cord injury (SCI) often leads to loss of locomotor function. Neuroplasticity of spinal circuitry underlies some functional recovery and therefore represents a therapeutic target to improve locomotor function following SCI. However, the cellular and molecular mechanisms mediating neuroplasticity below the lesion level are not fully understood. The present study performed a gene expression profiling in the rat lumbar spinal cord at 1 and 3 weeks after contusive SCI at T9. The below-level gene expression profiles were compared with those of animals that were subjected to treadmill locomotor training.
2013-11-27 | GSE52763 | GEO
Project description:Label-free mass spectrometry-based quantitative proteomics was applied to a larval zebrafish spinal cord injury model, which allows axon regeneration and functional recovery within two days (days post lesion; dpl) after a spinal cord transection in 3 day-old larvae (dpf). Proteomic profiling was performed of the lesion site at 1 dpl in control animals and animals with pdgfrb+ cell-specific overexpression of either zebrafish chondoradherin (chad; chad-mCherry fusion), fibromodulin a (fmoda; fmoda-mCherry fusion), lumican (lum; lum-mCherry fusion) or prolargin (prelp; prelp-mCherry fusion).
2023-09-06 | PXD037605 | Pride
Project description:Identification of temporal variations in miRNA expression after spinal cord injury caused by thoracic (T8) moderate (200 Kdynes) contusion. Expression changes were analyzed 1, 3 and 7 days after injury and compared to expression of control (untreated) and sham (laminectony but no contusion) individuals. Included groups: control (untreated), 1 day after lesion, 3 days after lesion, 7 days after lesion, 1 days after SHAM cirugy, 3 days after SHAM cirugy, and 7 days after SHAM cirugy. Each of these 7 groups included 5 biological replicates.
2011-07-01 | E-GEOD-19890 | biostudies-arrayexpress