Transglutaminase 2 gene ablation protects against renal ischemic injury by blocking constant NF-κB activation

Dae Seok Kim, Bora Kim, Hongmin Tahk, Dong Hyun Kim, Eu Ree Ahn, Changsun Choi, Yoon Jeon, Seo Young Park, Ho Lee, Seung Hyun Oh, Soo Youl Kim

Research output: Contribution to journalArticle

31 Scopus citations

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 languageEnglish (US)
Pages (from-to)479-484
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume403
Issue number3-4
DOIs
StatePublished - Dec 17 2010
Externally publishedYes

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

Fingerprint Dive into the research topics of 'Transglutaminase 2 gene ablation protects against renal ischemic injury by blocking constant NF-κB activation'. Together they form a unique fingerprint.

  • Cite this

    Kim, D. S., Kim, B., Tahk, H., Kim, D. H., Ahn, E. R., Choi, C., Jeon, Y., Park, S. Y., Lee, H., Oh, S. H., & Kim, S. Y. (2010). Transglutaminase 2 gene ablation protects against renal ischemic injury by blocking constant NF-κB activation. Biochemical and Biophysical Research Communications, 403(3-4), 479-484. https://doi.org/10.1016/j.bbrc.2010.11.063