@article{oai:nagasaki-u.repo.nii.ac.jp:00015244,
 author = {Nakayama, Seiko and Mukae, Hiroshi and Sakamoto, Noriho and Kakugawa, Tomoyuki and Yoshioka, Sumako and Soda, Hiroshi and Oku, Hisashi and Urata, Yoshie and Kondo, Takahito and Kubota, Hiroshi and Nagata, Kazuhiro and Kohno, Shigeru},
 issue = {3-4},
 journal = {Life sciences},
 month = {Jan},
 note = {Pirfenidone (5-methyl-1-phenyl-2-(1H)-pyridone) is a novel anti-fibrotic and anti-inflammatory agent that inhibits the progression of fibrosis in animal models and patients with idiopathic pulmonary fibrosis (IPF). Heat shock protein (HSP) 47, a collagen-specific molecular chaperone, is involved in the processing and/or secretion of procollagen and plays an important role in the pathogenesis of IPF. The present study evaluated the in vitro effects of pirfenidone on expression of HSP47 and collagen type I in cultured normal human lung fibroblasts (NHLF). Expression levels of HSP47 and collagen type I in NHLF stimulated by transforming growth factor (TGF)-beta1 were evaluated genetically, immunologically and immunocytochemically. Treatment with TGF-beta1 stimulated both mRNA and protein expressions of both HSP47 and collagen type I in NHLF, and pirfenidone significantly inhibited this TGF-beta1-enhanced expression in a dose-dependent manner. We concluded that the anti-fibrotic effect of pirfenidone may be mediated not only through direct inhibition of collagen type I expression but also at least partly through inhibition of HSP47 expression in lung fibroblasts, with a resultant reduction of collagen synthesis in lung fibrosis., Life sciences, 82(3-4), pp.210-217; 2008},
 pages = {210--217},
 title = {Pirfenidone inhibits the expression of HSP47 in TGF-beta1-stimulated human lung fibroblasts.},
 volume = {82},
 year = {2008}
}