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Pirfenidone inhibitsTGF-β1-inducedover-expression ofcollagen type I andheat shock protein 47in A549 cells Keiko HisatomiHiroshi MukaeNoriho Sakamoto2012 год

Pirfenidone inhibits TGF-β1-induced over-expression of collagen type I and heat shock protein 47 in A549 cells
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Аннотация: Abstract Background Pirfenidone is a novel anti-fibrotic and anti-inflammatory agent that inhibits the progression of fibrosis in animal models and in patients with idiopathic pulmonary fibrosis (IPF). We previously showed that pirfenidone inhibits the over-expression of collagen type I and of heat shock protein (HSP) 47, a collagen-specific molecular chaperone, in human lung fibroblasts stimulated with transforming growth factor (TGF)-β1 in vitro . The increased numbers of HSP47-positive type II pneumocytes as well as fibroblasts were also diminished by pirfenidone in an animal model of pulmonary fibrosis induced by bleomycin. The present study evaluates the effects of pirfenidone on collagen type I and HSP47 expression in the human alveolar epithelial cell line, A549 cells in vitro . Methods The expression of collagen type I, HSP47 and E-cadherin mRNAs in A549 cells stimulated with TGF-β1 was evaluated by Northern blotting or real-time PCR. The expression of collagen type I, HSP47 and fibronectin proteins was assessed by immunocytochemical staining. Results TGF-β1 stimulated collagen type I and HSP47 mRNA and protein expression in A549 cells, and pirfenidone significantly inhibited this process. Pirfenidone also inhibited over-expression of the fibroblast phenotypic marker fibronectin in A549 cells induced by TGF-β1. Conclusion We concluded that the anti-fibrotic effects of pirfenidone might be mediated not only through the direct inhibition of collagen type I expression but also through the inhibition of HSP47 expression in alveolar epithelial cells, which results in reduced collagen synthesis in lung fibrosis. Furthermore, pirfenidone might partially inhibit the epithelial-mesenchymal transition.
Год издания: 2012
Авторы: Keiko Hisatomi, Hiroshi Mukae, Noriho Sakamoto, Yuji Ishimatsu, Tomoyuki Kakugawa, Shintaro Hara, Hanako Fujita, Seiko Nakamichi, Hisashi Oku, Yoshishige Urata, Hiroshi Kubota, Kazuhiro Nagata, Shigeru Kohno
Издательство: BioMed Central
Источник: BMC Pulmonary Medicine
Ключевые слова: Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis, Occupational and environmental lung diseases, Occupational exposure and asthma
Другие ссылки: BMC Pulmonary Medicine (PDF)
BMC Pulmonary Medicine (HTML)
Europe PMC (PubMed Central) (PDF)
Europe PMC (PubMed Central) (HTML)
PubMed Central (HTML)
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