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Department of Internal Medicine, University of Iowa College of Medicine and Veterans Affairs Medical Center, Iowa City, IA 52243
Alveolar macrophages have been implicated in the pathogenesis of a
number of acute and chronic lung disorders. We have previously shown
that normal human alveolar macrophages exhibit decreased DNA binding
activity of the transcription factor, AP-1, compared with monocytes.
Furthermore, this decrease in AP-1 DNA binding appears to be due to a
decrease in the redox active protein, redox factor (Ref)-1. Ref-1 is an
important redox regulator of a number of transcription factors,
including NF-
B and AP-1. In this study we evaluated the role of
asbestos, a prototypic model of chronic fibrotic lung disease, in Ref-1
expression and activity. We found that incubation with low
concentrations of crocidolite asbestos (0.5–1.25 µg/cm2)
resulted in an increase in nuclear Ref-1 protein after 5 min, with a
persistent elevation in protein up to 24 h. Additionally, an
increase in nuclear Ref-1 could be induced by treating the cells with
an oxidant-generating stimulus (iron loading plus PMA) and inhibited by
diphenyleneiodonium chloride, an inhibitor of NADPH oxidase. The
asbestos-induced accumulation of nuclear Ref-1 was associated with an
increase in AP-1 DNA binding activity. These findings suggest that an
exposure associated with fibrotic lung disease, i.e., asbestos,
modulates accumulation of nuclear Ref-1 in macrophages, and that this
effect is mediated by an oxidant stimulus.
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