| First Author | Chen X | Year | 2012 |
| Journal | Biochem Biophys Res Commun | Volume | 428 |
| Issue | 3 | Pages | 327-32 |
| PubMed ID | 22995314 | Mgi Jnum | J:190095 |
| Mgi Id | MGI:5448071 | Doi | 10.1016/j.bbrc.2012.09.033 |
| Citation | Chen X, et al. (2012) Role of RNA-binding protein tristetraprolin in tumor necrosis factor-alpha mediated gene expression. Biochem Biophys Res Commun 428(3):327-32 |
| abstractText | Tumor necrosis factor-alpha (TNF-alpha) plays an important role in the pathogenesis of inflammatory diseases. Excessive TNF-alpha expression induces tristetraprolin (TTP), an RNA-binding protein that regulates mRNA degradation, which in turn downregulates TNF and its downstream genes, thus resulting in anti-inflammatory effects. In order to better understand the TNF-alpha mediated molecular pathways in inflammatory diseases, embryonic fibroblast (MEF) cell lines derived from TTP-deficient (KO) or wild type (WT) mice were treated with TNF-alpha and gene expression differences between two cell lines were compared by a microarray essay of 9224 genes. We found that TTP-KO cells had higher expression levels of pro-inflammatory genes than TTP-WT cells, and inflammatory genes were differentially regulated by TNF-alpha between TTP-KO and TTP-WT cells. Through a study of 2-dimentional gene set matrix analysis, we also found the genes upregulated by TNF-alpha in TTP KO cells were correlated with the pathologic phenotypes in inflammation, joint, or bone diseases. Our study provided a detailed genetic roadmap for further understanding the regulatory effect of TTP in inflammatory pathways related to human diseases. |
