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Am J Physiol Lung Cell Mol Physiol (February 20, 2004). doi:10.1152/ajplung.00394.2003
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Submitted on November 18, 2003
Accepted on February 12, 2004

Altered Bleomycin-Induced Lung Fibrosis in Osteopontin-Deficient Mice

Jeffrey S. Berman1, David Serlin2, Xinfang Li2, Geoffrey Whitley2, John Hayes3, David C. Rishikof2, Dennis A. Ricupero2, Lucy Liaw4, Margaret Goetschkes5, and Anthony W. O'Regan2*

1 The Pulmonary Center, Boston University School of Medicine, Boston, MA, USA; The Pulmonary Department, Boston Veterans Administration Medical Center, Boston, MA, USA
2 The Pulmonary Center, Boston University School of Medicine, Boston, MA, USA
3 Department of Pathology, Boston University School of Medicine, Boston, MA, USA
4 Center for Molecular Medicine, Maine Medical Center, Scarborough, ME, USA
5 Pathology Services, Inc, Cambridge, MA, USA

* To whom correspondence should be addressed. E-mail: aoregan{at}lung.bumc.bu.edu.

Osteopontin is a multifunctional matricellular protein abundantly expressed during inflammation and repair. Osteopontin deficiency is associated with abnormal wound repair characterized by aberrant collagen fibrillogenesis in the heart and skin. Recent gene microarray studies found that osteopontin is abundantly expressed in both human and mouse lung fibrosis. Macrophages and T cells are known to be major sources of osteopontin. During lung fibrosis, however, osteopontin expression continues to increase when inflammation has receded suggesting alternative sources of ostepontin during this response. In this study we demonstrate immunoreactivity for osteopontin in lung epithelial and inflammatory cells in human usual interstitial pneumonitis and murine bleomycin-induced lung fibrosis. Following treatment with bleomycin, osteopontin-null mice develop lung fibrosis characterized by dilated distal airspaces and reduced type I collagen expression compared to wild-type controls. There is also a significant decrease in levels of active TGF-{beta}1 and matrix metalloproteinase-2 in osteopontin null mice. Type III collagen expression and total collagenase activity is similar in both groups. These results demonstrate that osteopontin expression is associated with important fibrogenic signals in the lung and that the epithelium may be an important source of osteopontin during lung fibrosis.




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