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Originally published In Press as doi:10.1074/jbc.M202941200 on April 26, 2002
J. Biol. Chem., Vol. 277, Issue 27, 24225-24231, July 5, 2002
A Novel Pathway for Nickel-induced Interleukin-8
Expression*
Aaron
Barchowsky ,
Nicole V.
Soucy,
Kimberley A.
O'Hara,
John
Hwa,
Trisha L.
Noreault, and
Angeline S.
Andrew
From the Department of Pharmacology and Toxicology, Dartmouth
Medical School, Hanover, New Hampshire 03755
Inhalation of particulate nickel subsulfide
(Ni3S2) causes chronic active
inflammation and fibrosis of the lungs. However, the mechanisms for
these effects are not well understood. Therefore, cell culture
experiments with BEAS-2B human airway epithelial cells were conducted
to test the hypothesis that exposure to non-cytotoxic levels of
Ni3S2 induces expression of inflammatory
cytokines such as interleukin-8 (IL-8). Exposure to
Ni3S2 for 48 h was required to
significantly increase IL-8 protein levels. Transcriptional stimulation
of IL-8 mRNA levels preceded the increase in protein. Transient
exposure to soluble nickel sulfate failed to increase IL-8 mRNA.
Transfection with truncated IL-8 promoter constructs linked to the
luciferase gene demonstrated that nickel-induced IL-8 transcription
required 272 bp of the promoter relative to the transcriptional start
site. A 133-bp construct, containing cytokine and hypoxia-sensitive
AP-1, NF-IL6, and NF- B sites, was insufficient for induction by
nickel. Transfection with a dominant negative AP-1 construct or
mutation of the AP-1, GATA, or C/EBP sites in the 272-bp IL-8
promoter construct blocked induction by nickel. Inhibiting ERK,
phosphatidylinositol 3-kinase, but not p38 kinase,
diacylglycerol kinase, or hypoxia-inducible factor-1 , attenuated
nickel induction of IL-8. These studies indicate that nickel induced
IL-8 transcription through a novel pathway that requires both AP-1 and
non-traditional transcription factors.
*
This work was supported by the Superfund Basic Research
Program at Dartmouth (Grant ES07373) and the facilities of the Norris Cotton Cancer Center.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Dept. of Pharmacology
and Toxicology, Dartmouth Medical School, 7650 Remsen, Hanover, NH
03755-3835. Tel.: 603-650-1673; Fax: 603-650-1129; E-mail: barchowsky@dartmouth.edu.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.

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Copyright © 2002 by the American Society for Biochemistry and Molecular Biology.
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