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Am J Physiol Lung Cell Mol Physiol (September 12, 2003). doi:10.1152/ajplung.00083.2003
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Submitted on March 21, 2003
Accepted on September 12, 2003

Modulation of PDGF-C and PDGF-D expression during bleomycin-induced lung fibrosis

Ying Zhuo1, Jian Zhang1, Miguel Laboy1, and Joseph A. Lasky1*

1 Department of Medicine, Tulane University Health Sciences Center, New Orleans, LA, USA

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

PDGF isoforms are a family of polypeptides that bind to cell surface receptors and induce fibroblast proliferation and chemotaxis. The PDGF-A and -B chain isoforms have been implicated in fibroproliferative lung injury in animal models and in human disease. Two recently recognized PDGF polypeptides, PDGF-C and -D, differ from the PDGF-A and -B isoforms in that they require proteolytic cleavage before they can bind and activate the PDGF receptors. Our findings demonstrate that administration of bleomycin to murine lungs leads to a significant increase in PDGF-C mRNA expression and a significant decrease in PDGF-D mRNA expression. PDGF-C expression was localized to areas of lung injury by in situ hybridization and PDGF-C expression was not upregulated in the lungs of BALB/c mice that are resistant to bleomycin-induced lung fibrosis. Moreover, there is in vivo phosphorylation of the PDGF-receptor that binds PDGF-C in response to bleomycin administration. These observations strongly suggest a role for PDGF-C in bleomycin-induced pulmonary fibrosis.




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