Regulation of macrophage inflammatory protein-2 gene expression in response to 2,4-dinitrofluorobenzene in RAW 264.7 cells

被引:12
作者
Kim, Dongbum [1 ]
Kim, Jinho [2 ]
Kwon, Sanghoon [3 ]
Kim, Youy-Jin [3 ]
Lee, Soohyoung [3 ]
Lee, Younghee [4 ]
Seo, Jae-Nam [5 ]
Park, Cheung-Seog [6 ]
Park, Kui Lea [2 ]
Kwon, Hyung-Joo [1 ,3 ]
机构
[1] Hallym Univ, Ctr Med Sci Res, Gangwon, Chuncheon, South Korea
[2] Natl Inst Toxicol Res, Immunotoxicol Team, Seoul, South Korea
[3] Hallym Univ, Dept Microbiol, Chunchon, Gangwon, South Korea
[4] Chungbuk Natl Univ, Coll Nat Sci, Dept Biochem, Chungbuk, South Korea
[5] Hallym Univ, Coll Med, Dept Pathol, Chunchon, Gangwon, South Korea
[6] Kyung Hee Univ, Coll Med, Dept Microbiol, Seoul, South Korea
关键词
AP-1; DNFB; macrophages; MIP-2;
D O I
10.5483/BMBRep.2008.41.4.316
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:316 / 321
页数:6
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