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Early rotarod training aggravates injury and impairs functional recovery after spinal cord injury

ABSTRACT: Early rotarod training aggravates injury and impairs functional recovery after spinal cord injury

PROVIDER: PRJNA798021 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17645718_1.fastq.gz	Fastqsanger.gz
	SRR17645718_2.fastq.gz	Fastqsanger.gz
	SRR17645719_1.fastq.gz	Fastqsanger.gz
	SRR17645719_2.fastq.gz	Fastqsanger.gz
	SRR17645720_1.fastq.gz	Fastqsanger.gz

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Early rotarod training aggravates injury and impairs functional recovery after spinal cord injury

Project description:Mice with rotarod training showed significant differences in the expression of trophic factors and cytokines, histological repair, and functional recovery when compared with the mice without training. To exlore the potential mechanism, we applied the next-generation sequence to compare the transcriptome profile between two groups. We found that there were 1299 DEGs between two groups with 586 upregulated genes and 713 downregulated genes. GO enrichment analysis revealed that DEGs, especially the downregulated genes, were primarily associated with revascularization biological process like angiogenesis, regulation of vasculature development, regulation of angiogenesis, and cellular component including postsynapse, neuron to neuron synapse, etc. On the other hand, KEGG pathway analysis showed that those significantly altered genes, also downregulated DEGs in particular, were mainly enriched in the PI3K-Akt signaling pathway.

2023-07-17 | GSE193806 | GEO

Genome wide analysis of upper spinal cords with training after spinal cord hemisection injury

Project description:The goal of this study is to elucidate the influence of treadmill training on transcriptome of the upper lumbar spinal cord after thoracic spinal cord hemisection. mRNA profiles of spinal cords at 23 days-post injury with/without treadmill training were generated. The expression levels of 650 genes in the trained animal were increased ( > 2-fold) compared to untrained animals. Our study represents the detailed analysis of transcriptomes of spinal cord distal to the hemisected lesion after treadmill training, with biologic replicates, generated by RNA-seq technology.

2019-01-15 | GSE115156 | GEO

Genome wide analysis of lower spinal cords with training after spinal cord hemisection injury

Project description:The goal of this study is to elucidate the influence of treadmill training on transcriptome of the lower lumbar spinal cord after thoracic spinal cord hemisection. mRNA profiles of spinal cords at 23 days-post injury with/without treadmill training were generated. The expression levels of 650 genes in the trained animal were increased ( > 2-fold) compared to untrained animals. Our study represents the detailed analysis of transcriptomes of spinal cord distal to the hemisected lesion after treadmill training, with biologic replicates, generated by RNA-seq technology.

2024-05-21 | GSE115229 | GEO

Molecular responses in skeletal muscles following spinal cord injury and the effect of locomotor training

Project description:Spinal cord injury (SCI) is one of the most disabling health problems facing adults today. Locomotor training has been shown to induce substantial recovery in muscle size and muscle function in both transected and contusion injury animal models of SCI. The overall objective of this study is to implement genome wide expression profiling of skeletal muscle to define the molecular pathways associated with muscle remodeling after SCI and during locomotor training (TM). We profiled rat soleus of total 36 samples including controls; 3, 8 and 14 days after SCI; 8 and 14 days after SCI with locomotor treadmill training (TM).

2015-06-30 | E-GEOD-45550 | biostudies-arrayexpress

Molecular responses in skeletal muscles following spinal cord injury and the effect of locomotor training

2015-06-30 | GSE45550 | GEO

Gut dysbiosis impairs recovery after spinal cord injury.

Project description:The trillions of microbes that exist in the gastrointestinal tract have emerged as pivotal regulators of mammalian development and physiology. Disruption of this gut microbiome, a process known as dysbiosis, causes or exacerbates various diseases, but whether gut dysbiosis affects recovery of neurological function or lesion pathology after traumatic spinal cord injury (SCI) is unknown. Data in this study show that SCI increases intestinal permeability and bacterial translocation from the gut. These changes are associated with immune cell activation in gut-associated lymphoid tissues (GALTs) and significant changes in the composition of both major and minor gut bacterial taxa. Postinjury changes in gut microbiota persist for at least one month and predict the magnitude of locomotor impairment. Experimental induction of gut dysbiosis in naive mice before SCI (e.g., via oral delivery of broad-spectrum antibiotics) exacerbates neurological impairment and spinal cord pathology after SCI. Conversely, feeding SCI mice commercial probiotics (VSL#3) enriched with lactic acid-producing bacteria triggers a protective immune response in GALTs and confers neuroprotection with improved locomotor recovery. Our data reveal a previously unknown role for the gut microbiota in influencing recovery of neurological function and neuropathology after SCI.

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Genome wide analysis of upper spinal cords with training after spinal cord hemisection injury

Project description:Genome wide analysis of upper spinal cords with training after spinal cord hemisection injury

| PRJNA473983 | ENA

Genome wide analysis of lower spinal cords with training after spinal cord hemisection injury

Project description:Genome wide analysis of lower spinal cords with training after spinal cord hemisection injury

| PRJNA474208 | ENA

Gene expression profiles in the spinal cord below the lesion level and influence of treadmill locomotor training

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 compared to control rat that received sham injury (laminectomy). The below-level gene expression profiles were compared with those of animals that were subjected to treadmill locomotor training. Rat lumbar spinal cords were taken for the microarray analysis at 1 and 3 weeks after contusive spinal cord injury at the T9 level. Another group of rats received treadmill locomotor training for 3 weeks, and theirs spinal cords were harvested for the microarray. The changes in gene expression after spinal cord injury were analyzed at the two time points. The influence of treadmill locomotor training was evaluated by comparing gene expression profiles between animals with or without treadmill training.

2013-11-27 | E-GEOD-52763 | biostudies-arrayexpress

Microglia and macrophages promote corralling, wound compaction and recovery in spinal cord injury via Plexin-B2

Project description:Tissue repair after spinal cord injury (SCI) requires mobilization of immune and glial cells to form a protective barrier that seals the wound and facilitates debris clearing, inflammatory containment, and matrix compaction. This process involves corralling, wherein phagocytic immune cells become confined to the necrotic core surrounded by an astrocytic border. Here, we elucidate a temporally distinct gene signature in injury-activated microglia/macrophages (IAM), which engages axon guidance pathways. Plexin-B2 is upregulated in IAM, which is required for motosensory recovery after SCI. Plexin-B2 deletion in myeloid cells impairs corralling, leading to diffuse tissue damage, inflammatory spillover, and hampered axon regeneration. Corralling begins early and requires Plexin-B2 in both microglia and macrophages. Mechanistically, Plexin-B2 promotes microglia motility, steers IAM away from colliding cells, and facilitates matrix compaction. Our data thus establish Plexin-B2 as an important link that integrates biochemical cues and physical interactions of IAM with the injury microenvironment during wound healing.

2019-12-23 | GSE113566 | GEO

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