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http://hdl.handle.net/2445/123933
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DC Field | Value | Language |
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dc.contributor.author | Molina Molina, María | - |
dc.contributor.author | Machahua, Carlos | - |
dc.contributor.author | Vicens Zygmunt, Vanesa | - |
dc.contributor.author | Llatjós, Roger | - |
dc.contributor.author | Escobar, I. | - |
dc.contributor.author | Sala Llinas, Ernest | - |
dc.contributor.author | Luburich Hernaiz, Patricio | - |
dc.contributor.author | Dorca i Sargatal, Jordi | - |
dc.contributor.author | Montes Worboys, Ana | - |
dc.date.accessioned | 2018-07-25T10:40:59Z | - |
dc.date.available | 2018-07-25T10:40:59Z | - |
dc.date.issued | 2018-04-27 | - |
dc.identifier.uri | http://hdl.handle.net/2445/123933 | - |
dc.description.abstract | Background: Pirfenidone, a pleiotropic anti-fibrotic treatment, has been shown to slow down disease progression of idiopathic pulmonary fibrosis (IPF), a fatal and devastating lung disease. Rapamycin, an inhibitor of fibroblast proliferation could be a potential anti-fibrotic drug to improve the effects of pirfenidone. Methods: Primary lung fibroblasts from IPF patients and human alveolar epithelial cells (A549) were treated in vitro with pirfenidone and rapamycin in the presence or absence of transforming growth factor beta 1 (TGF-beta). Extracellular matrix protein and gene expression of markers involved in lung fibrosis (tenascin-c, fibronectin, collagen I (COM Al], collagen III [COL3A1] and alpha-smooth muscle actin [alpha-SMA]) were analyzed. A cell migration assay in pirfenidone, rapamycin and TGF-beta-containing media was performed. Results: Gene and protein expression of tenascin-c and fibronectin of fibrotic fibroblasts were reduced by pirfenidone or rapamycin treatment Pirfenidone-rapamycin treatment did not revert the epithelial to mesenchymal transition pathway activated by TGF-beta. However, the drug combination significantly abrogated fibroblast to myofibroblast transition. The inhibitory effect of pirfenidone on fibroblast migration in the scratch-wound assay was potentiated by rapamycin combination. Conclusions: These findings indicate that the combination of pirfenidone and rapamycin widen the inhibition range of fibrogenic markers and prevents fibroblast migration. These results would open a new line of research for an anti-fibrotic combination therapeutic approach. | - |
dc.format.extent | 13 p. | - |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.publisher | Biomed Central Ltd | - |
dc.relation.isformatof | Reproducció del document publicat a: https://doi.org/10.1186/s12890-018-0626-4 | - |
dc.relation.ispartof | Bmc Pulmonary Medicine, 2018, Vol. 18:63 | - |
dc.relation.uri | https://doi.org/10.1186/s12890-018-0626-4 | - |
dc.rights | cc-by (c) Molina-Molina, María et al., 2018 | - |
dc.rights.uri | http://creativecommons.org/licenses/by/3.0/es/ | * |
dc.source | Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL)) | - |
dc.subject.classification | Fibrosi pulmonar | - |
dc.subject.classification | Matriu extracel·lular | - |
dc.subject.classification | Terapèutica | - |
dc.subject.mesh | Therapeutics | - |
dc.subject.other | Pulmonary fibrosis | - |
dc.subject.other | Extracellular matrix | - |
dc.title | Anti-fibrotic Effects Of Pirfenidone And Rapamycin In Primary Ipf Fibroblasts And Human Alveolar Epithelial Cells | - |
dc.type | info:eu-repo/semantics/article | - |
dc.type | info:eu-repo/semantics/publishedVersion | - |
dc.date.updated | 2018-07-24T11:42:58Z | - |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | - |
dc.identifier.pmid | 29703175 | - |
Appears in Collections: | Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL)) |
Files in This Item:
File | Description | Size | Format | |
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Molina-MolinaM.pdf | 1.86 MB | Adobe PDF | View/Open |
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