Boldine increases functional recovery and response to physical rehabilitation in a mouse model of contusion spinal cord injury
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ABSTRACT:
PROVIDER: PRJNA911838 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22721167_1.fastq.gz | Fastqsanger.gz | |||
| SRR22721167_2.fastq.gz | Fastqsanger.gz | |||
| SRR22721168_1.fastq.gz | Fastqsanger.gz | |||
| SRR22721168_2.fastq.gz | Fastqsanger.gz | |||
| SRR22721169_1.fastq.gz | Fastqsanger.gz |
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Project description:Membrane channels such as connexins (Cx), pannexins and P2X7 receptors are permeable to calcium, ATP and other small molecules. Release of ATP and glutamate through these channels is a key mechanism driving tissue response to traumas such as spinal cord injury (SCI). Boldine, an alkaloid isolated from the Chilean boldo tree, blocks both Cx hemichannels and pannexins. To test if boldine improved function after SCI, boldine or vehicle was administered to mice with a moderate severity contusion SCI. Boldine increased spared white matter and locomotor function as determined by the Basso Mouse Scale and horizontal ladder rung walk tests. Increases in locomotor function observed after treadmill walking at a slow speed were further augmented by boldine. Boldine reduced immunostaining for activated microglia (Iba1) and astrocytic (GFAP) markers while increasing that for axon growth and neuroplasticity (GAP-43). Cell culture studies demonstrated that boldine blocked hemichannels, specifically Cx26 and Cx30, on cultured astrocytes and blocked calcium entry through activated P2X7R. Studies by RT-qPCR showed that boldine reduced expression of chemokine Ccl2, cytokine IL-6 and microglial gene CD68, while increasing expression of the neurotransmission genes SNAP25 and Grin2b, as well as GAP-43. Bulk RNA sequencing revealed that boldine modulated a large number of genes involved in neurotransmission in in spinal cord tissue just below the lesion epicenter at 14 days after SCI and that numbers of genes regulated by boldine was much lower at 28 days after injury. These results indicate that boldine spares tissue and increases locomotor function through mechanisms that may include reduced expression of pro-inflammatory molecules resulting in greater remodeling of surviving circuits
2023-07-12 | GSE220907 | GEO
Project description:Gene expression analysis after the treatments for functional recovery after contusion injury which are mediated by glutathione Experiment Overall Design: 24 hours after contusion and treatments Experiment Overall Design: Groups include normal, laminectomy, contusion and treatments on contused rats (clenbuterol, X-ray, tempol, BSO and tempol/BSO)
2008-06-13 | E-GEOD-5273 | biostudies-arrayexpress
Project description:Excerpt from a larger study which characterized the transcriptional effects of a spinal cord contusion injury in rats. This is the data from the almost chronic contusion state (35 days) at the injury site (Thoracic 8) - where we saw significant changes in several areas, including cholesterol metabolism genes. Other spinal cord areas (rostral, caudal) and time-points (3 hours, 24 hours, 7 days and 35 days) were analyzed as well and are discussed in our paper and at www.crpf.org/microarray. Keywords = Spinal Cord Injury Keywords = chronic Keywords = thoracic Keywords = cholesterol Keywords: repeat sample
2005-05-03 | GSE2599 | GEO
Project description:Gene expression analysis after the treatments for functional recovery after contusion injury which are mediated by glutathione Keywords: treatment
2006-07-12 | GSE5273 | GEO
Project description:Excerpt from a larger study which characterized the transcriptional effects of a spinal cord contusion injury in rats. This is the data from the almost chronic contusion state (35 days) at the injury site (Thoracic 8) - where we saw significant changes in several areas, including cholesterol metabolism genes. Other spinal cord areas (rostral, caudal) and time-points (3 hours, 24 hours, 7 days and 35 days) were analyzed as well and are discussed in our paper and at www.crpf.org/microarray.
2007-10-08 | E-GEOD-2599 | biostudies-arrayexpress
Project description:T cells undergo autoimmunization following spinal cord injury (SCI) and play both protective and destructive roles during the recovery process. T-cell deficient athymic nude (AN) rats recover better than immunocompetent Sprague-Dawley (SD) rats following spinal cord transection. In the present study, we evaluated locomotor recovery in SD and AN rats following moderate spinal cord contusion. To explain variable locomotor outcome, we assessed whole-genome expression using RNA sequencing, in the acute (1 week post-injury) and chronic (8 weeks post-injury) phases of recovery. AN rats demonstrated greater locomotor function than SD rats only at 1 week post-injury, coinciding with peak T cell infiltration in immunocompetent rats. Genetic markers for T cells and helper T cells were acutely enriched in SD rats, while AN rats expressed genes for Th2 cells, cytotoxic T cells, NK cells, mast cells, IL-1a, and IL-6 at higher levels. Acute enrichment of cell death-related genes suggested that SD rats undergo secondary tissue damage from T cells. Additionally, SD rats exhibited increased acute expression of voltage-gated potassium (Kv) channel-related genes. However, AN rats demonstrated greater chronic expression of cell death-associated genes and less expression of axon-related genes. We put forth a model in which T cells facilitate early tissue damage, demyelination, and Kv channel dysregulation in SD rats following contusion SCI. However, compensatory features of the immune response in AN rats cause delayed tissue death and limit long-term recovery. T cell inhibition combined with other neuroprotective treatment may thus be a promising therapeutic avenue. 2x2 model with 4 groups and 12 total samples. 2 rat strains (athymic nude [AN] and Sprague-Dawley [SD]) and 2 time points (1 week post-injury [acute] and 8 weeks post-injury [chronic]). 3 samples per group, for a total of 12 samples. No technical replicates were performed. Acute SD group = rats 618, 619, and 620. Chronic SD group = rats 605, 606, and 608. Acute AN group = rats 714, 715, and 717. Chronic AN group = rats 707, 712, and 713.
2015-10-26 | E-GEOD-62760 | biostudies-arrayexpress
Project description:T cells undergo autoimmunization following spinal cord injury (SCI) and play both protective and destructive roles during the recovery process. T-cell deficient athymic nude (AN) rats recover better than immunocompetent Sprague-Dawley (SD) rats following spinal cord transection. In the present study, we evaluated locomotor recovery in SD and AN rats following moderate spinal cord contusion. To explain variable locomotor outcome, we assessed whole-genome expression using RNA sequencing, in the acute (1 week post-injury) and chronic (8 weeks post-injury) phases of recovery. AN rats demonstrated greater locomotor function than SD rats only at 1 week post-injury, coinciding with peak T cell infiltration in immunocompetent rats. Genetic markers for T cells and helper T cells were acutely enriched in SD rats, while AN rats expressed genes for Th2 cells, cytotoxic T cells, NK cells, mast cells, IL-1a, and IL-6 at higher levels. Acute enrichment of cell death-related genes suggested that SD rats undergo secondary tissue damage from T cells. Additionally, SD rats exhibited increased acute expression of voltage-gated potassium (Kv) channel-related genes. However, AN rats demonstrated greater chronic expression of cell death-associated genes and less expression of axon-related genes. We put forth a model in which T cells facilitate early tissue damage, demyelination, and Kv channel dysregulation in SD rats following contusion SCI. However, compensatory features of the immune response in AN rats cause delayed tissue death and limit long-term recovery. T cell inhibition combined with other neuroprotective treatment may thus be a promising therapeutic avenue.
2015-10-26 | GSE62760 | GEO
Project description:Axons fail to regenerate in the injured spinal cord, limiting motor and autonomic recovery and contributing to long-term morbidity. Endogenous inhibitors, including those on residual myelin, contribute to regeneration failure. One inhibitor, myelin-associated glycoprotein (MAG), binds to sialoglycans and other receptors on axons. MAG inhibition of axon outgrowth in some neurons is reversed by treatment with sialidase, an enzyme that hydrolyzes sialic acids and eliminates MAG-sialoglycan binding. We delivered recombinant sialidase intrathecally to rats following a spinal cord contusive injury. Sialidase (or saline solution) was infused to the injury site continuously for 2 wk and then motor behavior, autonomic physiology, and anatomic outcomes were determined 3 wk later. Sialidase treatment significantly enhanced hindlimb motor function, improved bulbospinally mediated autonomic reflexes, and increased axon sprouting. These findings validate sialoglycans as therapeutic targets and sialidase as a candidate therapy for spinal cord injury.
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Project description:Hyperbaric oxygen therapy after mid-cervical spinal contusion injury
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Project description:Unpublished findings related to Frontiers 2021 article: Fully characterized mature human iPS- and NMP-derived motor neurons thrive without neuroprotection in the spinal contusion cavity
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