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Cerebrovascular Disease and Ischemia

開催日 2014/9/13
時間 11:00 - 12:00
会場 Poster / Exhibition(Event Hall B)

Overrepresented transcription factor binding sites identified following an animal model of ischemic stroke

  • P3-339
  • Monique Surles Zeigler:1 Yonggang Li:1 Alicia S Gates:1 Byron Ford:1 
  • 1:Neuroscience Institute, Morehouse School of Medicine, Atlanta, USA 

Ischemic stroke is a major cause of morbidity and mortality both globally and domestically. The neurological damage associated with ischemic stroke has been shown to involve an uncontrolled, unresolved inflammatory response activating and/or repressing several groups of genes that are regulated by transcription factors. The identification of transcription factors regulating inflammation following ischemic stroke may ultimately lead to the development of more effective therapies. Sprague-Dawley rats were allocated to 2 groups, ischemia (permanent middle cerebral artery occlusion (pMCAO)) and sham surgery control. Sham rats underwent the same surgery procedure as the ischemia group, but were not subjected to pMCAO. Rats were sacrificed 24 hours after surgery, brain tissue was collected, and RNA was isolated and prepared for microarray analysis. The data set produced by Affymetrix software contained gene identifiers and the corresponding expression values. This data was analyzed in Microsoft Excel for calculation of average and fold change. Gene expression values that increased by 4-fold or more following pMCAO when compared to sham and were present in either all ischemia samples or all sham samples were identified. This gene set was uploaded to Pathway Studio bioinformatics software for further data analysis. Conserved Transcription Factor Binding Site Finder (CONFAC) web-based bioinformatics software was used to identify transcription factors that were overrepresented for this dataset. Preliminary studies identified inflammatory response as the top biological function in ischemic brain tissue. Transcription factors such as Oct-1 and NRF-2 are overrepresented for this dataset and may play a role in the regulation of inflammatory genes following ischemic stroke. Potential therapies to reduce the detrimental effects of ischemic stroke may involve the modulation these transcription factors.

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