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Am J Physiol Lung Cell Mol Physiol (October 18, 2002). doi:10.1152/ajplung.00115.2002
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Articles in PresS, published online ahead of print October 18, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00115.2002
Submitted on April 16, 2002
Accepted on October 11, 2002

Haptoglobin reduces lung injury associated with exposure to blood

Funmei Yang1*, David J. Haile2, Franklin G. Berger3, Damon C. Herbert1, Emily Van Beveren1, and Andrew J. Ghio4

1 Department of Cellular and Structural Biology, University of Texas Health Science Center, San Antonio, Texas, USA
2 Department of Medicine, University of Texas Health Science Center, San Antonio, Texas, USA
3 Department of Biological Sciences, University of South Carolina, Columbia, South Carolina, USA
4 NHEERL, Human Studies Division, Environmental Protection Agency, Chapel Hill, North Carolina, USA

* To whom correspondence should be addressed. E-mail: Yangf{at}uthscsa.edu.

The biological functions of the acute phase protein haptoglobin (Hp) may be related to its ability to bind hemoglobin (Hb) or to modulate immune response. Hp is expressed at a high level in lung cells; yet, its protective role(s) in the lung is not known. Using transgenic mice overexpressing Hp in alveolar macrophages, we demonstrated that Hp diminished Hb-induced lung injury when the lung was exposed to whole blood. In transgenic mouse lungs, hemoglobin was more efficiently removed and the induction of stress responsive heme oxygenase 1 (HO-1) gene was significantly lower when compared to the wild type mice. At 24 hours after blood treatment, the ferritin level that serves as an index for intracellular iron content was also lower in alveolar macrophages in transgenic mice than in wild type mice. We propose that an Hp-mediated Hb catabolism process exists in alveolar macrophages. This process is likely coupled to an iron mobilization pathway and may be an efficient mechanism to reduce oxidative damage associated with hemolysis.




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