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E-GEOD-51566 - Effect of experimental stroke on meningeal gene expression and the influence of mast cells on these gene changes
Released on 31 July 2014, last updated on 2 August 2014
Stroke is a leading cause of adult disability and death. Inflammation plays an important role in stroke pathology, but the factors which promote brain inflammation in this setting remain to be fully defined. Here we investigate the meninges, the membranes that envelop the brain, for a potential role in modulating immune cell trafficking to the brain. We also investigate the potential of mast cells (MCs) to modulate this response as MCs are often considered as 'first responders' playing a critical role in the initiation and development of inflammation in many disease settings. We find that stroke increases expression of inflammatory and immune response genes in the meninges in mice consistent with a potential role in modulating immune cell trafficking. Moreover, genetic and cell transfer approaches identify MCs as important modulators of this response. Three categories of male mice were used: wild-type (WT) mice, mast cell-deficient (KO) mice, and mast cell-engrafted mice (EN), which are mast cell-deficient mice repaired of their mast cell deficiency by engraftment of mast cells i.v. 8-10 weeks prior to experimentation. The mouse strain was WBB6F1-Kit+/+ (wild-type ) and WBB6F1-KitW/W-v (mast cell-deficient ). Each mouse category was subdivided into two groups, naïve (N) and stroke (S), with n=3 per group. The stroke model was 30 minute filament occlusion of the middle cerebral artery. The dura were removed from the mouse brains at 2d post-stroke and from aged-matched naïve mice for microarray analysis. Dura were not pooled but run on separate arrays.
transcription profiling by array
Ahmet Arac, Anna Tsykin, Gary K Steinberg, Gregory J Goodall, Michele A Grimbaldeston, Stephen J Galli, Tonya M Bliss, Ulrich Schlecht