| Autor: |
Azuma A; Fourth Department of Internal Medicine, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113, Japan. a-azuma@nms.ac.jp, Li YJ, Abe S, Usuki J, Matsuda K, Henmi S, Miyauchi Y, Ueda K, Izawa A, Sone S, Hashimoto S, Kudoh S |
| Jazyk: |
angličtina |
| Zdroj: |
American journal of respiratory cell and molecular biology [Am J Respir Cell Mol Biol] 2005 Feb; Vol. 32 (2), pp. 93-8. Date of Electronic Publication: 2004 Nov 19. |
| DOI: |
10.1165/rcmb.2003-0374OC |
| Abstrakt: |
Pulmonary fibrosis is the result of abnormal processes of repair that occur after lung injury. Transforming growth factor (TGF)-beta is a key molecule in the progression of pulmonary fibrosis. Although clinical use of interferon (IFN)-beta did not improve survival in patients with idiopathic pulmonary fibrosis, because some preclinical studies have suggested that IFN-beta is a potent inhibitor of fibrogenesis, beneficial effects of IFN-beta have been expected. We therefore attempted to determine effects of IFN-beta and investigated the mechanism of action of IFN-beta in bleomycin-induced pulmonary fibrosis. Bleomycin at Day 0 and IFN-beta for 4 wk were administered intravenously to ICR mice. At 28 d after bleomycin injection, histologic and chemical analysis was performed for evaluation of effects of IFN-beta. Tissue distribution and amounts of TGF-beta1 and thrombospondin (TSP)-1/2 were analyzed. IFN-beta attenuated prolylhydroxylase activity, resulting in inhibition of pulmonary fibrosis. Bleomycin-induced increase in TGF-beta1 in epithelial cells and extracellular matrix was attenuated by IFN-beta. TSP-1/2 was limited in platelets of control mice, but was present in foamy cells in fibrotic regions induced by bleomycin. These findings suggest that the antifibrotic effect of IFN-beta is inhibition of TGF-beta and its activation via decrease in TSP-1/2 in lung tissue and change in location of TSP-1/2 from platelets to foamy cells. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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