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Effect of Hepatocyte Growth Factor on Lung Injury and Development of Clinical Application*

Kenichi Akiyama, MD; M. Miki, MD; K. Narumi, MD; M. Ebina, MD; M. Yaekashiwa, MD; A. Nakamura, MD; T. Nakamura, MD; T. Nukiwa, MD
Author and Funding Information

*From the Department of Respiratory Oncology and Molecular Medicine, Institute of Development, Aging, and Cancer, Tohuko University, Sendai, Japan; and the Division of Biochemistry, Department of Oncology, Biomedical Research Center, Osaka University Medical School, Osaka, Japan.

Correspondence to: Kenichi Akiyama, MD, Department of Respiratory Oncology and Molecular Medicine, Institute of Development, Aging, and Cancer, Tohuku University, 4-1 Seiryomachi Aoba-ku, Sendai 980-8575, Japan



Chest. 2001;120(1_suppl):S59. doi:10.1378/chest.120.1_suppl.S59
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Hepatocyte growth factor (HGF) is a humoral mediator of epithelial-mesenchymal interactions, acting on a variety of epithelial cells. In our previous studies, higher HGF levels were detected in the BAL fluid of patients with pulmonary fibrosis,1 and HGF could prevent the progression of bleomycin-induced lung fibrosis in mice using human recombinant HGF.2 To step up the clinical application of HGF for respiratory diseases, we examined the adenoviral-mediated HGF treatment. While the intratracheal administration of adenoviral vector expressing rat HGF (AdCAG.HGF) yielded high transient HGF expression (312.5 ng/g lung tissue, day 3), adenovirus caused neutrophil alveolitis. In spite of indirect intraperitoneal administration of AdCAG.HGF (6 × 108 pfu) to C57BL/6 mice with bleomycin-induced lung injury, reduced hydroxyproline content (128 ± 5%; n = 5, day 28) resulted in AdCAG.HGF-treated mice, compared with mice treated with adenovirus without complementary DNA insertion (177 ± 9%, p < 0.005). Furthermore, the alveolar apoptotic cells in bleomycin-induced lung injury determined by deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling stain was also reduced by the intraperitoneal administration of AdCAG.HGF (35 ± 4% vs 13 ± 1%; p < 0.05). These results indicate the potential therapeutic effect of HGF for lung injury and fibrosis, and thus await the development of the clinical administration.

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