BMB Reports

생화학분자생물학회 (Korean Society for Biochemistry and Molecular Biology)
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Regulation of macrophage inflammatory protein-2 gene expression in response to 2,4-dinitrofluorobenzene in RAW 264.7 cells

  • Kim, Dong-Bum (Center for Medical Science Research, Hallym University) ;
  • Kim, Jin-Ho (Immunotoxicology Team, National Institute of Toxicological Research) ;
  • Kwon, Sang-Hoon (Department of Microbiology, Hallym University) ;
  • Kim, Young-Jin (Department of Microbiology, Hallym University) ;
  • Lee, Soo-Hyoung (Department of Microbiology, Hallym University) ;
  • Lee, Young-Hee (Department of Biochemistry, College of Natural Sciences, Chungbuk National University) ;
  • Seo, Jae-Nam (Department of Pathology, College of Medicine, Hallym University) ;
  • Park, Cheung-Seog (Department of Microbiology, College of Medicine, Kyung Hee University) ;
  • Park, Kui-Lea (Immunotoxicology Team, National Institute of Toxicological Research) ;
  • Kwon, Hyung-Joo (Center for Medical Science Research, Hallym University)
  • 투고 : 2007.10.01
  • 심사 : 2007.11.18
  • 발행 : 2008.04.30
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초록

Several skin sensitizers, like 2,4-dinitrofluorobenzene (DNFB), are known to provoke contact hypersensitivity responses after topical application. Here, we show that DNFB can upregulate macrophage inflammatory protein-2 (MIP-2) expression in RAW 264.7 cells via a mechanism that is largely dependent on mitogen-activated protein kinase (MAPK) signaling pathways. ELISA-based transcription factor activation assays and chromatin immunoprecipitation assays revealed that functional interaction between AP-1 and MIP-2 promoter element is necessary for MIP-2 gene expression by DNFB. Interestingly, topical application of DNFB to NC/Nga mice increased MIP-2 expression in dermis, suggesting that MIP-2 contributes to the leukocyte infiltration associated with atopic dermatitis. These results provide additional insight of the mechanism of contact hypersensitivity induced by contact sensitizers.

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참고문헌

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