Browsing by Author "Brandan, Enrique"
Now showing 1 - 20 of 118
Results Per Page
Sort Options
- ItemA high molecular weight proteoglycan is differentially expressed during development of the mollusc Concholepas concholepas (Mollusca; Gastropoda; Muricidae)(1992) Brandan, Enrique; Inestrosa Cantín, Nibaldo
- ItemA Lipid- Anchoret Heparan Sulfate Proteoglycan Is Present in the Suface of Differentiated Skeletal Muscle Cells. Isolation and Biochemical Characterization(1993) Campos, A.; Konig Samohod, Cecilia; Brandan, Enrique
- ItemA Novel Mechanism of Sequestering FGF-2 by Glypican in Lipid Rafts, Allowing Skeletal Muscle Differentiation(2010) Gutiérrez Pérez, Jaime Agustín; Brandan, Enrique
- ItemA novel modulatory mechanism of transforming growth factor-ss signaling through decorin and LRP-1(2007) Cabello Verrugio, Claudio Alejandro; Brandan, Enrique
- ItemACE2 is augmented in dystrophic skeletal muscle and plays a role in decreasing associated fibrosis(2014) Riquelme Illanes, Cecilia Angélica; Acuna, M.; Torrejon, J.; Rebolledo, D.; Cabrera, D.; Santos, R.; Brandan, Enrique
- ItemAdenovirus-mediated hepatic syndecan-1 overexpression induces hepatocyte proliferation and hyperlipidaemia in mice(2007) Cortés, V.; Zanlungo Matsuhiro, Silvana; Brandan, Enrique; Rigotti Rivera, Attilio
- ItemAdherent muscle connective tissue fibroblasts are phenotypically and biochemically equivalent to stromal fibro/adipogenic progenitors(2019) Contreras Saavedra, Osvaldo Isaías; Rossi, Fabio M.; Brandan, Enrique
- ItemALS skeletal muscle shows enhanced TGF-β signaling, fibrosis and induction of fibro/adipogenic progenitor markers.(2017) Gonzalez, David; Contreras Saavedra, Osvaldo Isaías; Brandan, Enrique; Rebolledo López, Daniela Victoria; Espinoza, Juan Pablo; Zundert, Brigitte van
- ItemAnalysis of Pathological Activities of CCN2/CTGF in Muscle Dystrophy(2017) Acuña, Maria José; Brandan, Enrique
- ItemAndrographolide Ameliorates Inflammation and Fibrogenesis and Attenuates Inflammasome Activation in Experimental Non-Alcoholic Steatohepatitis(2017) Cabrera, Daniel; Wree, Alexander; Povero, Davide; Solís, Nancy; Hernández, Alejandra; Pizarro Rojas, Margarita Alicia; Moshage, Han; Torres Montes, Paula Javiera; Feldstein, Ariel E.; Cabello Verrugio, Claudio Alejandro; Brandan, Enrique; Barrera Martínez, Francisco Javier; Arab Verdugo, Juan Pablo; Arrese Jiménez, Marco
- ItemAndrographolide attenuates skeletal muscle dystrophy in mdx mice and increases efficiency of cell therapy by reducing fibrosis(2014) Cabrera, D.; Gutiérrez, J.; Cabello Verrugio, Claudio Alejandro; Morales, M. G.; Mezzano, S.; Fadic Ruiz, Ricardo Julio Nicolás; Casar Leturia, Juan Carlos; Hancke, J. L.; Brandan, EnriqueBackground: Duchenne muscular dystrophy (DMD) is characterized by the absence of the cytoskeletal protein dystrophin, muscle wasting, increased transforming growth factor type beta (TGF-β) signaling, and fibrosis. At the present time, the only clinically validated treatments for DMD are glucocorticoids. These drugs prolong muscle strength and ambulation of patients for a short term only and have severe adverse effects. Andrographolide, a bicyclic diterpenoid lactone, has traditionally been used for the treatment of colds, fever, laryngitis, and other infections with no or minimal side effects. We determined whether andrographolide treatment of mdx mice, an animal model for DMD, affects muscle damage, physiology, fibrosis, and efficiency of cell therapy.Methods: mdx mice were treated with andrographolide for three months and skeletal muscle histology, creatine kinase activity, and permeability of muscle fibers were evaluated. Fibrosis and TGF-β signaling were evaluated by indirect immunofluorescence and Western blot analyses. Muscle strength was determined in isolated skeletal muscles and by a running test. Efficiency of cell therapy was determined by grafting isolated skeletal muscle satellite cells onto the tibialis anterior of mdx mice.Results: mdx mice treated with andrographolide exhibited less severe muscular dystrophy than untreated dystrophic mice. They performed better in an exercise endurance test and had improved muscle strength in isolated muscles, reduced skeletal muscle impairment, diminished fibrosis and a significant reduction in TGF-β signaling. Moreover, andrographolide treatment of mdx mice improved grafting efficiency upon intramuscular injection of dystrophin-positive satellite cells.Conclusions: These results suggest that andrographolide could be used to improve quality of life in individuals with DMD.
- ItemAngiotensin II receptor type 1 blockade decreases CTGF/CCN2-mediated damage and fibrosis in normal and dystrophic skeletal muscles(2012) Cabello Verrugio, Claudio Alejandro; Morales France, María Gabriela; Vio Lagos, Carlos P.; Brandan, Enrique
- ItemAngiotensin II-induced pro-fibrotic effects require p38MAPK activity and transforming growth factor beta 1 expression in skeletal muscle cells(2012) Morales France, María Gabriela; Brandan, Enrique; Cabello Verrugio, Claudio Alejandro
- ItemAngiotensin-(1-7) attenuates disuse skeletal muscle atrophy in mice via its receptor, Mas(2016) Morales, M. G.; Abrigo, J.; Acuña M. J.; Santos, Ra.; Bader, M.; Brandan, Enrique; Simon, F.; Olguín Marín, Hugo César; Cabrera, D.; Cabello Verrugio, Claudio Alejandro
- ItemAngiotensin-(1-7) prevents lipopolysaccharide-induced autophagy via the mas receptor in skeletal muscle(2020) Rivera, J. C.; Abrigo, J.; Tacchi, F.; Simón, F.; Brandan, Enrique; Santos, R. A.; Bader, M.; Chiong, M.; Cabello Verrugio, Claudio Alejandro
- ItemAngiotensins as therapeutic targets beyond heart disease(2015) Passos Silva, Danielle Gomes; Brandan, Enrique; Souza Santos, Robson Augusto
- ItemAntisense Inhibition of Decorin Expression in Myoblasts Decreases Cell Responsiveness to Transforming Growth Factor B and Accelerates Skeletal Muscle Defferentiation(Elsevier Inc, 2001) Riquelme Illanes, Cecilia Angélica; Larraín Correa, Juan Agustín; Schönherr, Elke; Henríquez, Juan Pablo; Kresse, Hans; Brandan, EnriqueDecorin is a member of the family of the small leucine-rich proteoglycans. In addition to its function as an extracellular matrix organizer, it has the ability to activate the epidermal growth factor receptor, and it forms complexes with various isoforms of transforming growth factor beta (TGF-beta), Decorin is expressed during skeletal muscle differentiation and is up-regulated in dystrophic muscle. In this study we investigated the role of decorin in TGF-beta -dependent inhibition of myogenesis, To probe the function of decorin during myogenesis, C2C12 myoblasts were stably transfected with a plasmid expressing antisense decorin mRNA. The re; suiting inhibition of decorin expression led to the expression of myogenin, a master transcription factor for muscle differentiation, under growth conditions and accelerated skeletal muscle differentiation as determined by the expression of creatine kinase, In contrast myogenin expression was inhibited by adenovirally induced decorin expression or by adding exogenous decorin, Reduced synthesis of decorin resulted in a 7-fold decreased sensitivity to TGF-beta -mediated inhibition of myogenin expression. In contrast, adenovirally induced decorin expression in wild type cells resulted in a 5-fold increased sensitivity to TGF-beta -mediated inhibition of myogenin expression. Transfection studies with the TGF-beta -dependent promoter of the plasminogen activator inhibitor-1 coupled with luciferase revealed that the transducing receptors for TGF-beta1 and TGF-beta2 were involved in the different responses of wild type and anti-sense decorin myoblasts, These results demonstrate that a reduction of decorin expression or of decorin availability results in a decreased responsiveness to TGF-beta. These findings strongly suggest a new role for decorin during skeletal muscle terminal differentiation by activating TGF-beta -dependent signaling pathways.
- ItemAspectos Biotecnológicos en Larvas de Loco(1990) Brandan, Enrique; Inestrosa Cantín, Nibaldo; Labarca Baeza, Rodrigo Claudio