Involvement of L-type Ca2+ Channel and Toll-Like Receptor-4 in Nickel-Induced Interleukin-8 Gene Expression

Chia Hsien Lin, Chih Ang Chung, Jhen Hong Wong, Ben Kuen Chen, Siou Jin Chiu, Sukhontip Klahan, Yi Chao Lee, Wei-Chiao Chang

研究成果: 雜誌貢獻文章同行評審

6 引文 斯高帕斯(Scopus)


The metal nickel (Ni2+) is found everywhere in our daily lives, including coins, costume jewelry, and even nuts and chocolates. Nickel poisoning can cause inflammatory reactions, respiratory diseases, and allergic contact dermatitis. To clarify the mechanism by which nickel induces mediators of inflammation, we used the human acute monocytic leukemia THP-1 cell line as a model. Interleukin (IL)-8 promoter activity as well as gene expression were tested by luciferase assay and real-time polymerase chain reaction. The underlying mechanisms of nickel-induced IL-8 were investigated. We found that nickel induced IL-8 gene expression via the L-type Ca2+ channel, Toll-like receptor-4 (TRL-4) and nuclear factor NF-κB signal transduction pathways. Nickel activated NF-κB expression through extracellular signal-regulated kinase 1/2 phosphorylation and then increased IL-8 expression. Thus, the L-type Ca2+ channel and TRL-4 play important roles in nickel-induced inflammatory gene expressions.
頁(從 - 到)5-12
期刊Environmental Toxicology
出版狀態已發佈 - 一月 1 2016

ASJC Scopus subject areas

  • Health, Toxicology and Mutagenesis
  • Toxicology
  • Management, Monitoring, Policy and Law

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