Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 403, Issue 3-4, Pages 479-484Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2010.11.063
Keywords
Transglutaminase 2; Transglutaminase 2 knockout mouse; Unilateral ureteral obstruction; Ischemia; Nuclear factor-kappa B; Renal injury
Categories
Funding
- National Cancer Center in Korea [NCC0510270, NCC0810181]
- Pioneer Research Center [20100002209]
- Ministry of Education, Science, and Technology [20090086078]
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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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