Proceedings of the Korean Society of Toxicology Conference (한국독성학회:학술대회논문집)

Korean Society of Toxicology & Korea Environmental Mutagen Society (한국독성학회)
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Induction of nuclear factor-${\kappa}B$ activation through TAK1 and NIK by diesel exhaust particles in L2 cell lines

  • Yun, Young-Pil (Department of Occupational and Environmental Medicine, St. Mary's Hospital, The Catholic University of Korea) ;
  • Joo, Jin-Deok (Department of Anesthesiology, Saint Vincent's Hospital, The Catholic University of Korea) ;
  • Lee, Joo-Yong (Catholic Neuroscience Center, The Catholic University of Korea) ;
  • Nam, Hae-Yun (Department of Occupational and Environmental Medicine, St. Mary's Hospital, The Catholic University of Korea) ;
  • Kim, Young-Hoon (Catholic Neuroscience Center, The Catholic University of Korea) ;
  • Lee, Kweon-Haeng (Catholic Neuroscience Center, The Catholic University of Korea, Department of Pharmacology, College of Medicine, The Catholic University of Korea) ;
  • Lim, Cheol-Soo (Environmental Research Complex) ;
  • Kim, Hyung-Jung (Department of Internal Medicine, College of Medicine, Yonsei University) ;
  • Lim, Yong-Gul (Department of Anesthesiology, Saint Vincent's Hospital, The Catholic University of Korea) ;
  • Lim, Young (Department of Occupational and Environmental Medicine, St. Mary's Hospital, The Catholic University of Korea)
  • Published : 2005.05.13
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Abstract

Diesel exhaust Particles (DEPs) are known to induce allergic responses in airway epithelial cells, such as the production of various cytokines via nuclear factor-kappa B ($NF-{\kappa}B$). However. the intracellular signal transduction pathways underlying this phenomenon have not been fully examined. This study showed that DEP induced $NF-{\kappa}B$ activity via transforming growth factor-${\beta}$ activated kinase 1 (TAK1) and $NF-{\kappa}B$-inducing kinase (NIK) in L2 rat lung epithelial cells. DEP induced the $NF-{\kappa}B$ dependent reporter activity approximately two-to three-fold in L2 cells. However, this effect was abolished by the expression of the dominant negative forms of TAK1 or NIK. Furthermore, it was shown that DEP induced TAK1 phosphorylation in the L2 cells. These results suggest that TAK1 and NIK are important mediators of DEP-induced $NF-{\kappa}B$ activation.

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