Abstract
Molecular mechanisms behind increased cerebral vasospasm and local inflammation in late cerebral ischemia after subarachnoid hemorrhage (SAH) are poorly elucidated. Using system biology tools and experimental SAH models, we have identified signal transducer and activator of transcription 3 (STAT3) transcription factor as a possible major regulatory molecule. On the basis of the presence of transcription factor binding sequence in the promoters of differentially regulated genes (significant enrichment PE: 6 × 10(5)) and the consistent expression of STAT3 (mRNA, P=0.0159 and Protein, P=0.0467), we hypothesize that unphosphorylated STAT3 may directly DNA bind and probably affect the genes that are involved in inflammation and late cerebral ischemia to influence the pathologic progression of SAH.
| Original language | English |
|---|---|
| Journal | Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism |
| Volume | 34 |
| Issue number | 5 |
| Pages (from-to) | 759-63 |
| Number of pages | 5 |
| ISSN | 0271-678X |
| DOIs | |
| Publication status | Published - May 2014 |
Keywords
- Animals
- Binding Sites
- Brain
- Brain Ischemia
- Gene Expression Regulation
- Gene Regulatory Networks
- Janus Kinase 2
- Male
- Phosphorylation
- Promoter Regions, Genetic
- Rats
- Rats, Sprague-Dawley
- STAT3 Transcription Factor
- Subarachnoid Hemorrhage
- Transcriptional Activation