| First Author | Kim DS | Year | 2010 |
| Journal | Biochem Biophys Res Commun | Volume | 403 |
| Issue | 3-4 | Pages | 479-84 |
| PubMed ID | 21094133 | Mgi Jnum | J:167049 |
| Mgi Id | MGI:4867102 | Doi | 10.1016/j.bbrc.2010.11.063 |
| Citation | Kim DS, et al. (2010) Transglutaminase 2 gene ablation protects against renal ischemic injury by blocking constant NF-kappaB activation. Biochem Biophys Res Commun 403(3-4):479-84 |
| abstractText | Transglutaminase 2 knockout (TGase2(-/-)) mice show significantly reduced inflammation with decreased myofibroblasts in a unilateral ureteral obstruction (UUO) model, but the mechanism remains to be clarified. Nuclear factor-kappaB (NF-kappaB) activation plays a major role in the progression of inflammation in an obstructive nephropathy model. However, the key factors extending the duration of NF-kappaB activation in UUO are not known. In several inflammatory diseases, we and others recently found that TGase 2 plays a key role in extending NF-kappaB activation, which contributes to the pathogenesis of disease. In the current study, we found that NF-kappaB activity in mouse embryogenic fibroblasts (MEFs) from TGase2(-/-) mice remained at the control level while the NF-kappaB activity of wild-type (WT) MEFs was highly increased under hypoxic stress. Using the obstructive nephropathy model, we found that NF-kappaB activity remained at the control level in TGase2(-/-) mouse kidney tissues, as measured by COX-2 expression, but was highly increased in WT tissues. We conclude that TGase 2 gene ablation reduces the duration of NF-kappaB activation in ischemic injury. |
