Transcriptional change of the lesion site margins after spinal cord injury in canine
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1136153 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29837764_1.fastq.gz | Fastqsanger.gz | |||
| SRR29837764_2.fastq.gz | Fastqsanger.gz | |||
| SRR29837765_1.fastq.gz | Fastqsanger.gz | |||
| SRR29837765_2.fastq.gz | Fastqsanger.gz | |||
| SRR29837766_1.fastq.gz | Fastqsanger.gz |
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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
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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.
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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.
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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.
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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.
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