Dataset Information


Comparative gene expression analysis of thoracic spinal cord from G93A SOD1 mutant rats and from wild type littermates following mild compression injury

ABSTRACT: In this study we investigate how the molecular response to a mechanical stress applied to the spinal cord can be modified by a G93A SOD1 gene mutation, a genetic defect known to cause an invariably fatal form of motor neuron disease. In a 7-day post-injury time period, we perform a 4 time points gene expression profiling of injured spinal cords obtained from pre-symptomatic rats over-expressing the G93A SOD1 gene mutation and from wild type (WT) littermates. The hypothesis tested in this investigation is that the presence of a known genetic defect in a pre-symptomatic rat with a macroscopically normal spinal cord modifies the molecular response to mechanical stress as part of an increase genetically-induced vulnerability to this kind of stress. A better understanding of the molecular mechanisms underlying this susceptibility to trauma may open the way to the uncovering of molecular events which are crucially linked to neurodegenerastion. Overall design: Total RNA was isolated from the spinal cords of both wild type (WT) and mutant (G93A SOD1 gene mutation) rats sacrificed after mild compression spinal cord injury (SCI) at 30 minutes, 4 hours, 24 hours and 7 days from the experimental injury. Total RNA was also isolated from the spinal cords of both wild type (WT) and mutant (G93A SOD1 gne mutation) rats sacrificed after sham operation at 30 minutes and 4 hours after surgery. RNA samples from rats spinal cords of the same genetic type sacrificed at the same time points after sham operation or compression SCI were pooled together, for a tota of 12 pooled samples.

INSTRUMENT(S): Illumina ratRef-12 v1.5.0.34 expression beadchip


PROVIDER: GSE22161 | GEO | 2010-06-05



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