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Genome-Wide Gene Expression Profiling of Spinal Cord Injury in Rat

ABSTRACT: The aneurysm clip impact-compression model of spinal cord injury (SCI) in animals mimics the primary mechanism of SCI in human, i.e. acute impact and persisting compression; and its histo-pathological and behavioural outcomes are extensively similar to the human SCI. In order to understand the distinct molecular events underlying this injury model, an analysis of global gene expression of the acute, subacute and chronic stages of a moderate to severe injury to the rat spinal cord was conducted using a microarray gene chip approach. Rat thoracic spinal cord (T7) was injured using aneurysm clip impact-compression injury model and the epicenter area of injured spinal cord was isolated for RNA extraction and processing and hybridization on Affymetrix GeneChip arrays.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Mahmood Chamankhah

PROVIDER: E-GEOD-45006 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome-Wide Gene Expression Profiling of Spinal Cord Injury in Rat

Project description:The aneurysm clip impact-compression model of spinal cord injury (SCI) in animals mimics the primary mechanism of SCI in human, i.e. acute impact and persisting compression; and its histo-pathological and behavioural outcomes are extensively similar to the human SCI. In order to understand the distinct molecular events underlying this injury model, an analysis of global gene expression of the acute, subacute and chronic stages of a moderate to severe injury to the rat spinal cord was conducted using a microarray gene chip approach.

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Project description:Traumatic spinal cord injury (SCI) may induce irreversible damage leading to severe incapacity. Molecular mechanisms underlying SCI are not fully understood, preventing the development of novel therapeutic resources. Tamoxifen has demonstrated to be a promising therapy. Our aim was to elucidate the molecular mechanisms involved in the beneficial effect of TMX administered after SCI. We use a rat model of SCI, Tamoxifen was administred intraperitoneal 30 min after injury. Four groups were organized, 1) Non-injured without TMX (Sham/TMX-), 2) Non-injured with TMX (Sham/TMX+), 3) Injured without TMX (SCI/TMX-), and 4) Injured with TMX (SCI/TMX+). From the comparison between Sham/TMX- and SCI/TMX-, 708 genes showed differential expression. Among the relevant genes Anxa1 was upregulated, this gene’s product is a promising marker of injury severity. Enriched pathways were the spinal cord injury pathway and pathways related to inflammatory response. When comparing SCI/TMX- versus SCI/TMX+, only 30 genes showed differential expression. Our results reinforce the key role of inflammatory response in SCI and Tamoxifen seem to be able to regulate this response by suppressing changes in gene expression. Our data also support the potential of previously described severity markers.

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Hyperbaric oxygen therapy after mid-cervical spinal contusion injury

Project description:Hyperbaric oxygen (HBO) therapy is frequently used to treat peripheral wounds or decompression sickness. Evidence suggests that HBO therapy can provide neuroprotection and has an anti-inflammatory impact after neurologic injury including spinal cord injury (SCI). Our primary purpose was to conduct an unbiased, genome-wide screening of mRNA expression changes in the injured spinal cord after HBO therapy. A mRNA gene array was used to evaluate samples taken from the contused region of the spinal cord following a lateralized mid-cervical contusion injury in adult female rats. HBO therapy consisted of daily, 1-hour sessions (3.0 ATA, 100% O2) initiated on the day of SCI. Gene set enrichment analyses indicated that HBO upregulated genes in pathways associated with electron transport, mitochondrial function, and oxidative phosphorylation, and downregulation genes in pathways associated with inflammation (including cytokines and NF-B) and apoptotic signaling. In a separate cohort, spinal cord histology was performed to verify whether the HBO treatment impacted neuronal cell counts or inflammatory markers. Compared to untreated rats, there was increased NeuN positive cells in the spinal cord of HBO treated rats (p=0.007). Further, staining for anti-ionized calcium binding adaptor protein (Iba-1, a microglial marker) was reduced after HBO (p=0.028). We conclude that HBO therapy, initiated shortly after SCI and continued for 10-days, can alter the molecular signature of the lesioned spinal cord in a manner consistent with an anti-inflammatory and neuroprotective impact.

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Transcription profiling time series of Rattus norvegicus raphe magnus and sensorimotor cortex samples following moderate spinal cord injury

Project description:Summary: Spinal cord injury (SCI) is a damage to the spinal cord induced by trauma or disease resulting in a loss of mobility or feeling. SCI is characterized by a primary mechanical injury followed by a secondary injury in which several molecular events are altered in the spinal cord often resulting in loss of neuronal function. Analysis of the areas directly (spinal cord) and indirectly (raphe and sensorimotor cortex) affected by injury will help understanding mechanisms of SCI. Hypothesis: Areas of the brain primarily affected by spinal cord injury are the Raphe and the Sensorimotor cortex thus gene expression profiling these two areas might contribute understanding the mechanisms of spinal cord injury. Specific Aim: The project aims at finding significantly altered genes in the Raphe and Sensorimotor cortex following an induced moderate spinal cord injury in T9.

2007-10-08 | E-GEOD-2270 | biostudies-arrayexpress

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