Abstract
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-κB (NF-κB) activation plays a major role in the progression of inflammation in an obstructive nephropathy model. However, the key factors extending the duration of NF-κB 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-κB activation, which contributes to the pathogenesis of disease. In the current study, we found that NF-κB activity in mouse embryogenic fibroblasts (MEFs) from TGase2-/- mice remained at the control level while the NF-κB activity of wild-type (WT) MEFs was highly increased under hypoxic stress. Using the obstructive nephropathy model, we found that NF-κB 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-κB activation in ischemic injury.
Original language | English (US) |
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Pages (from-to) | 479-484 |
Number of pages | 6 |
Journal | Biochemical and Biophysical Research Communications |
Volume | 403 |
Issue number | 3-4 |
DOIs | |
State | Published - Dec 17 2010 |
Externally published | Yes |
Keywords
- Ischemia
- Nuclear factor-κB
- Renal injury
- Transglutaminase 2
- Transglutaminase 2 knockout mouse
- Unilateral ureteral obstruction
ASJC Scopus subject areas
- Biophysics
- Biochemistry
- Molecular Biology
- Cell Biology