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The Enhanced Monocyte Adhesiveness after UVB Exposure Requires ROS and NF-κB Signaling in Human Keratinocyte

  • Park, Lee-Jin (Department of Biomedical Science, Hallym University) ;
  • Ju, Sung-Mi (Department of Biomedical Science, Hallym University) ;
  • Song, Ha-Yong (Department of Biomedical Science, Hallym University) ;
  • Lee, Ji-Ae (Department of Biomedical Science, Hallym University) ;
  • Yang, Mi-Young (Department of Biomedical Science, Hallym University) ;
  • Kang, Young-Hee (Department of Food and Nutrition, College of Medicine, Hallym University) ;
  • Kwon, Hyung-Joo (Department of Microbiology, College of Medicine, Hallym University) ;
  • Kim, Tae-Yoon (Research Institutes of Medical Science, The Catholic University of Korea) ;
  • Choi, Soo-Young (Department of Biomedical Science, Hallym University) ;
  • Park, Jin-Seu (Department of Biomedical Science, Hallym University)
  • Received : 2006.05.09
  • Accepted : 2006.06.08
  • Published : 2006.09.30

Abstract

The infiltration of both monocyte and activated T cells in the skin is one of critical steps in the development of UVB-induced inflammation. Upregulation of adhesion molecules such as intercellular adhesion molecule 1 (ICAM-1) on the surface of keratinocytes plays an important role in this process. In this study, we examined the molecular mechanism responsible for UVB-induced expression of ICAM-1 and subsequent monocyte adhesion by keratinocyte. We observed that (1) UVB induced protein and mRNA expression of ICAM-1 in a dose- and time-dependent manner in human keratinocyte cell HaCaT; (2) UVB induced the translocation of NF-kappaB and inhibition of NF-kappaB by NF-kappaB inhibitors suppressed UVB-induced mRNA and protein expression of ICAM-1; (3) UVB increased the intracellular level of reactive oxygen species (ROS) by HaCaT cells; (4) UVB-induced increase of intracellular ROS level was suppressed by pre-treatment with diphenyl iodonium (DPI) and N-acetyl cysteine (NAC); and (5) inhibition of UVB-induced ROS production by DPI or NAC suppressed UVB-mediated translocation of NF-kappaB, expression of ICAM-1 and subsequent monocyte adhesion in HaCaT cells. These results suggest that UVB-induced ROS is involved in the translocation of NF-kappaB which is responsible for expression of ICAM-1 and subsequent increased monocyte adhesion in human keratinocyte.

Keywords

References

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