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Dadun > Depósito Académico > CIMA (Centro de Investigación Médica Aplicada) > Área de Terapia génica y Hepatología > Inmunología experimental > DA - CIMA - Terapia génica y Hepatología - Inmunología experimental - Artículos de revista >

Therapeutic effect of a peptide inhibitor of TGF-β on pulmonary fibrosis
Autor(es) : Arribillaga, L. (Laura)
Dotor, J. (Javier)
Basagoiti, M. (María)
Riezu-Boj, J.I. (José Ignacio)
Borras-Cuesta, F. (Francisco)
Lasarte, J.J. (Juan José)
Sarobe, P. (Pablo)
Cornet, M.E. (María Eugenia)
Feijoo, E. (Esperanza)
Palabras clave : Myofibroblasts
Peptide
Pulmonary fibrosis
Transforming growth factor-β1
Fecha incorporación: 2011
Editorial : Elsevier
Versión del editor: http://www.sciencedirect.com/science/article/pii/S1043466610007696
ISSN: 1096-0023
Cita: Arribillaga L, Dotor J, Basagoiti M, Riezu-Boj JI, Borras-Cuesta F, Lasarte JJ, et al. Therapeutic effect of a peptide inhibitor of TGF-beta on pulmonary fibrosis. Cytokine 2011 Mar;53(3):327-333.
Resumen
Pulmonary fibrosis encompasses several respiratory diseases characterized by epithelial cell injury, inflammation and fibrosis. Transforming growth factor (TGF)-β1 is one of the main profibrogenic cytokines involved in the pathogenesis of lung fibrosis. It induces fibroblast differentiation into myofibroblasts, which produce high levels of collagen and concomitantly loss of lung elasticity and reduction of the respiratory function. In the present study, we have investigated the effects of P17 (a TGF-β inhibitor peptide) on IMR-90 lung fibroblast differentiation in vitro, as well as on the inhibition of the development of bleomycin-induced pulmonary fibrosis in mice. It was found that in IMR-90 cells, P17 inhibited TGF-β1-induced expression of connective tissue growth factor and α-smooth muscle actin. In vivo, treatment of mice with P17 2days after bleomycin administration decreased lung fibrosis, areas of myofibroblast-like cells and lymphocyte infiltrate. P17 also reduced mRNA expression of collagen type I, fibronectin and the fibronectin splice isoform EDA in the lung, and increased the expression of IFN-γ mRNA. Finally, therapeutic treatment with P17 in mice with already established fibrosis was able to significantly attenuate the progression of lung fibrosis. These results suggest that P17 may be useful in the treatment of pulmonary fibrosis.
Enlace permanente: http://hdl.handle.net/10171/21580
Aparece en las colecciones: DA - CUN - Medicina interna - Artículos de revista
DA - CIMA - Terapia génica y Hepatología - Virología - Artículos de revista
DA - Medicina - Medicina Interna - Artículos de revista
DA - CIMA - Terapia génica y Hepatología - Inmunología hepatitis virales - Artículos de revista
DA - CIMA - Terapia génica y Hepatología - Inmunología experimental - Artículos de revista

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