Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 하헌주 | * |
dc.date.accessioned | 2018-06-06T08:13:14Z | - |
dc.date.available | 2018-06-06T08:13:14Z | - |
dc.date.issued | 2005 | * |
dc.identifier.issn | 0378-0066 | * |
dc.identifier.other | OAK-17467 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/244716 | - |
dc.description.abstract | Background: The transforming growth factor-β1 (TGF-β1) plays a key role in lung fibrosis. However, the molecular mechanisms involved in TGF-β1-induced lung fibrosis are unclear. TGF-β1 is the key inducer of myofibroblast transdifferentiation via de novo synthesis of α-smooth muscle actin (α-SMA). Since TGF-β1 signals through reactive oxygen species (ROS) and ROS have been shown to induce accumulation of extracellular matrix (ECM) in various tissues, this study examined if ROS play a role in TGF-β1-induced fibronectin secretion and α-SMA expression in human lung fibroblasts, MRC-5 cells. Methods: Growth arrested and synchronized MRC-5 cells were stimulated with TGF-β1 (0.2-10 ng/ml) in the presence or absence of N-acetylcysteine (NAC) or diphenyleneiodonium (DPI) for up to 96 hours. Dichlorofluorescein (DCF)-sensitive cellular ROS were measured by FACScan and secreted fibronectin and cellular α-SMA by Western blot analysis. Results: TGF-β1 increased the level of fibronectin secretion and α-SMA expression in MRC-5 cells in a dose-dependent manner. Both NAC (20 and 30 mM) and DPI (1 and 5 μM) significantly inhibited TGF-β1-induced fibronectin and α-SMA upregulation. The TGF-β1-induced cellular ROS level was also significantly reduced by NAC and DPI. Conclusions: The results suggest that NADPH oxidase-dependent ROS play an important role in TGF-β1-induced fibronectin secretion and α-SMA expression in MRC-5 cells, which leads to myofibroblast transdifferentiation and progressive lung fibrosis. | * |
dc.language | Korean | * |
dc.title | Role of reactive oxygen species in transforming growth factor-β1- inuduced fibronectin secretion and α-smooth muscle actin expression in human lung fibroblasts | * |
dc.type | Article | * |
dc.relation.issue | 3 | * |
dc.relation.volume | 58 | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 267 | * |
dc.relation.lastpage | 275 | * |
dc.relation.journaltitle | Tuberculosis and Respiratory Diseases | * |
dc.identifier.scopusid | 2-s2.0-20344377188 | * |
dc.author.google | Ha H. | * |
dc.author.google | Yu M.-R. | * |
dc.author.google | Uh S.-T. | * |
dc.author.google | Park C.S. | * |
dc.author.google | Lee H.B. | * |
dc.contributor.scopusid | 하헌주(7202277106) | * |
dc.date.modifydate | 20240422113229 | * |