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KMID : 0380220060390050618
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Journal of Biochemistry and Molecular Biology
2006 Volume.39 No. 5 p.618 ~ p.625
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The Enhanced Monocyte Adhesiveness after UVB Exposure Requires ROS and NF-κB Signaling in Human Keratinocyte
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Park Lee-Jin
Ju Sung-Mi
Song Ha-Yong
Lee Ji-Ae
Yang Mi-Young
Kang Young-Hee
Kwon Hyung-Joo
Kim Tae-Yoon
Choi Soo-Young
Park Jin-Seu
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Abstract
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The infiltration of both monocyte and activated T cells in the skin is one of critical steps in the development of UVBinduced 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 UVBinduced 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 pretreatment 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.
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KEYWORD
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Adhesion, ICAM-1, Inflammation, NF-κB, ROS, UV
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