Pirfenidone inhibits the expression of HSP47 in TGF-beta1-stimulated human lung fibroblasts
| العنوان: | Pirfenidone inhibits the expression of HSP47 in TGF-beta1-stimulated human lung fibroblasts |
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| المؤلفون: | Hiroshi Mukae, Tomoyuki Kakugawa, Hiroshi Soda, Yoshie Urata, Sumako Yoshioka, Shigeru Kohno, Takahito Kondo, Noriho Sakamoto, Hiroshi Kubota, Hisashi Oku, Seiko Nakayama, Kazuhiro Nagata |
| المصدر: | Life sciences. 82(3-4):210-217 |
| بيانات النشر: | Elsevier Inc., 2008. |
| سنة النشر: | 2008 |
| مصطلحات موضوعية: | Pyridones, Blotting, Western, Gene Expression, Idiopathic pulmonary fibrosis, Pirfenidone, General Biochemistry, Genetics and Molecular Biology, Cell Line, Transforming Growth Factor beta1, Collagen type I, Fibrosis, Heat shock protein, medicine, Humans, RNA, Messenger, General Pharmacology, Toxicology and Pharmaceutics, Fibroblast, HSP47 Heat-Shock Proteins, Lung, Dose-Response Relationship, Drug, Chemistry, Anti-Inflammatory Agents, Non-Steroidal, General Medicine, Fibroblasts, Blotting, Northern, medicine.disease, Immunohistochemistry, Procollagen peptidase, medicine.anatomical_structure, Cell culture, Heat shock protein 47 (HSP47), Immunology, Cancer research, Lung fibrosis, Drug Antagonism, medicine.drug, Transforming growth factor |
| الوصف: | 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 |
| وصف الملف: | application/pdf |
| اللغة: | English |
| تدمد: | 0024-3205 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::bd23da24d9c04578fa393c9795f7063aTest http://hdl.handle.net/10069/23124Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....bd23da24d9c04578fa393c9795f7063a |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 00243205 |
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