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Articles in PresS, published online ahead of print June 14, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00114.2002
Submitted on April 16, 2002
Accepted on May 16, 2002
1 Department of Cellular and Structural Biology, University of Texas Health Science Center, San Antonio, Texas, USA
2 Center for Environmental Medicine and Lung Biology, University of North Carolina, Chapel Hill, North Carolina, USA
3 Department of Medicine, University of Texas Health Science Center, San Antonio, Texas, USA
4 Department of Medicine, Duke University, Durham, North Carolina, USA
5 NHEERL, Human Studies Division, Environmental Protection Agency, Chapel Hill, North Carolina, USA
* To whom correspondence should be addressed. E-mail: Ghio.andy{at}epa.gov.
Accumulation of reactive iron in acute and chronic lung disease suggests iron driven free radical formation could contribute to tissue injury. Safe transport and sequestration of this metal is likely to be of importance in lung defense. We provide evidence for the expression and iron-induced upregulation of the metal transporter protein 1 (MTP1) genes in human and rodent lung cells at both protein and mRNA levels. In human bronchial epithelial cells, a 3.8-fold increase in mRNA level and a 2.4-fold increase in protein level of MTP1 were observed after iron exposure. In freshly isolated human macrophages, as much as an 18-fold increase in the MTP1 protein level was detected after incubation with an iron compound. The elevation in expression of MTP1 gene was also demonstrated in iron-instilled rat lungs and in hypotransferrinemic mouse lung. This is similar to our previous findings on divalent metal transporter 1 (DMT1), an iron transporter required for iron uptake and intracellular iron trafficking. These studies suggest the presence of iron mobilization and/or detoxification pathways in the lung that are crucial for iron homeostasis and lung defense.
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