Transglutaminase 2 gene ablation protects against renal ischemic injury by blocking constant NF-kappa B activation
- Authors
- Kim, Dae-Seok; Kim, Bora; Tahk, Hongmin; Kim, Dong-Hyun; Ahn, Eu-Ree; Choi, Changsun; Jeon, Yoon; Park, Seo Young; Lee, Ho; Oh, Seung Hyun; Kim, Soo-Youl
- Issue Date
- Dec-2010
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- Transglutaminase 2; Transglutaminase 2 knockout mouse; Unilateral ureteral obstruction; Ischemia; Nuclear factor-kappa B; Renal injury
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.403, no.3-4, pp 479 - 484
- Pages
- 6
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 403
- Number
- 3-4
- Start Page
- 479
- End Page
- 484
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/22008
- DOI
- 10.1016/j.bbrc.2010.11.063
- ISSN
- 0006-291X
1090-2104
- 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-kappa B (NF-kappa B) activation plays a major role in the progression of inflammation in an obstructive nephropathy model. However, the key factors extending the duration of NF-kappa B 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-kappa B activation, which contributes to the pathogenesis of disease. In the current study, we found that NF-kappa B activity in mouse embryogenic fibroblasts (MEFs) from TGase2(-/-) mice remained at the control level while the NF-kappa B activity of wild-type (WT) MEFs was highly increased under hypoxic stress. Using the obstructive nephropathy model, we found that NF-kappa B 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-kappa B activation in ischemic injury. (C) 2010 Elsevier Inc. All rights reserved.
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