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Articles in PresS, published online ahead of print February 15, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00187.2001
Submitted on May 29, 2001
Accepted on February 12, 2002
1 Department of Molecular Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, Japan
2 National Kinki Chuou Hospital for Chest Disease, Sakai, Osaka, Japan
* To whom correspondence should be addressed. E-mail: matsuoka{at}imed3.med.osaka-u.ac.jp.
To elucidate the pathophysiology of pulmonary fibrosis, we investigate the involvement of p38 mitogen-activated protein kinase (MAPK), which is one of major signal transduction pathways of proinflammatory cytokines, in a murine model of bleomycin-induced lung fibrosis. p38 MAPK and its substrate, activating transcription factor (ATF)-2, in bronchoalveolar lavage fluid (BALF) cells was phosphorylated by intratracheal exposure of bleomycin, and the phosphorylation of ATF-2 was inhibited by subcutaneous administration of a specific inhibitor of p38 MAPK, FR167653. FR167653 also inhibited augmented expression of tumor necrosis factor (TNF)-
, connective tissue growth factor (CTGF), and apoptosis of lung cells induced by bleomycin administration. Moreover, daily subcutaneous administration of FR167653 (from one day before to 14 days after bleomycin administration) ameliorated pulmonary fibrosis and pulmonary cachexia induced by bleomycin. These findings demonstrated that p38 MAPK is involved in bleomycin-induced pulmonary fibrosis and its inhibitor, FR167653, may be a feasible therapeutic agent.
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