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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-
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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