Browsing by Author "Cabello Verrugio, Claudio Alejandro"
Now showing 1 - 20 of 35
Results Per Page
Sort Options
- ItemA novel modulatory mechanism of transforming growth factor-ss signaling through decorin and LRP-1(2007) Cabello Verrugio, Claudio Alejandro; 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
- ItemAngiotensin-(1-7) Prevents Skeletal Muscle Atrophy Induced by Transforming Growth Factor Type Beta (TGF-beta) via Mas Receptor Activation(2016) Abrigo, Johanna; Simon, Felipe; Cabrera García, Daniel Alejandro; Cabello Verrugio, Claudio Alejandro
- ItemBetaglycan expression is transcriptionally up-regulated during skeletal muscle differentiation: Cloning of murine betaglycan gene promoter and its modulation by myoD, retinoic acid, and transforming growth factor-beta(Elsevier Inc., 2003) López-Casillas, Fernando; Riquelme Illanes, Cecilia Angélica; Pérez-Kato, Yoshiaki; Ponce-Castañeda, M. Verónica; Osses Rivera, Nelson Eduardo; Esparza-López, José; González-Núñez, Gerardo; Cabello Verrugio, Claudio Alejandro; Mendoza, Valentín; Troncoso, Víctor; Brandan, EnriqueBetaglycan is a membrane-anchored proteoglycan co-receptor that binds transforming growth factor beta (TGF-beta) via its core protein and basic fibroblast growth factor through its glycosaminoglycan chains. In this study we evaluated the expression of betaglycan during the C2C12 skeletal muscle differentiation. Betaglycan expression, as determined by Northern and Western blot, was up-regulated during the conversion of myoblasts to myotubes. The mouse betaglycan gene promoter was cloned, and its sequence showed putative binding sites for SP1, Smad3, Smad4, muscle regulatory factor elements such as MyoD and MEF2, and retinoic acid receptor. Transcriptional activity of the mouse betaglycan promoter reporter was also up-regulated in differentiating C2C12 cells. We found that MyoD, but not myogenin, stimulated this transcriptional activity even in the presence of high serum. Betaglycan promoter activity was increased by RA and inhibited by the three isoforms of TGF-beta. On the other hand, basic fibroblast growth factor, BMP-2, and hepatocyte growth factor/scatter factor, which are inhibitors of myogenesis, had little effect. In myotubes, up-regulated betaglycan was also detectable by TGF-beta affinity labeling and immunofluorescence microscopy studies. The latter indicated that betaglycan was localized both on the cell surface and in the ECM Forced expression of betaglycan in C2C12 myoblasts increases their responsiveness to TGF-beta2, suggesting that it performs a TGF-beta presentation function in this cell lineage. These results indicate that betaglycan expression is up-regulated during myogenesis and that MyoD and RA modulate its expression by a mechanism that is independent of myogenin.
- ItemCentral Role of Transforming Growth Factor Type Beta 1 in Skeletal Muscle Dysfunctions: An Update on Therapeutic Strategies(2018) Abrigo, Johanna; Simon, Felipe; Cabrera, Daniel; Cordova, Gonzalo; Trollet, Capucine; Cabello Verrugio, Claudio Alejandro
- ItemCholic acid and deoxycholic acid induce skeletal muscle atrophy through a mechanism dependent on TGR5 receptor(2020) Abrigo, J.; Gonzalez, F.; Aguirre, F.; Tacchi, F.; Gonzalez, A.; Meza, M. P.; Simon, F.; Cabrera García, Daniel Alejandro; Arrese, Marco; Karpen, S.; Cabello Verrugio, Claudio Alejandro
- ItemConnective tissue growth factor induction by lysophosphatidic acid requires transactivation of transforming growth factor type beta receptors and the JNK pathway(2011) Cabello Verrugio, Claudio Alejandro; Zúñiga Cóndor, Lidia Miriam; Brandan, Enrique
- ItemCTGF/CCN-2 over-expression can directly induce features of skeletal muscle dystrophy(2011) Morales France, María Gabriela; Cabello Verrugio, Claudio Alejandro; Santander Sepúlveda, Cristian Andrés; Cabrera García, Daniel Alejandro; Roel Goldschmeding; Brandan, Enrique
- ItemDiet-Induced Nonalcoholic Fatty Liver Disease Is Associated with Sarcopenia and Decreased Serum Insulin-Like Growth Factor-1(2016) Cabrera, D.; Ruiz, A.; Cabello Verrugio, Claudio Alejandro; Brandan, Enrique; Estrada, L.; Pizarro, M.; Solis, N.; Torres Montes, Paula Javiera; Barrera Martínez, Francisco José; Arrese Jiménez, Marco
- ItemEndothelial-to-mesenchymal transition: Cytokine-mediated pathways that determine endothelial fibrosis under inflammatory conditions(2017) Kalergis Parra, Alexis Mikes; Pérez, L.; Muñoz, N.; Riedel, C.; Echeverría, C.; Cabello Verrugio, Claudio Alejandro; Simon, F.
- ItemEndotoxin-Induced Endothelial Fibrosis Is Dependent on Expression of Transforming Growth Factors beta 1 and beta 2(2014) Echeverría, César; Montorfano, Ignacio; Tapia, Pablo; Riedel, Claudia; Cabello Verrugio, Claudio Alejandro; Simon, Felipe
- ItemEndotoxin-induced skeletal muscle wasting is prevented by angiotensin-(1-7) through a p38 MAPK-dependent mechanism(2015) Morales, María Gabriela; Olguín Marín, Hugo César; Di Capua, Gabriella; Brandan, Enrique; Simon, Felipe; Cabello Verrugio, Claudio Alejandro; Morales, María Gabriela; Olguín Marín, Hugo César; Di Capua, Gabriella; Brandan, Enrique; Simon, Felipe; Cabello Verrugio, Claudio Alejandro
- ItemEndotoxin-induced vascular endothelial cell migration is dependent on TLR4/NF-¿B pathway, NAD(P)H oxidase activation, and transient receptor potential melastatin 7 calcium channel activity(2014) Sarmiento, D.; Montorfano, I.; Cáceres, M.; Echeverría, C.; Fernández, R.; Cabello Verrugio, Claudio Alejandro; Cerda, O.; Tapia, Pablo; Simón, F.
- ItemExtracellular Proteoglycans Modify Tgf-Beta Bio-Availability Attenuating Its Signaling During Skeletal Muscle Differentiation(Elsevier, 2006) Droguett Mallea, Rebeca Antonia; Cabello Verrugio, Claudio Alejandro; Riquelme Illanes, Cecilia Angélica; Brandan, Enrique
- ItemFibrotic response induced by angiotensin-II requires NAD(P)H oxidase-induced reactive oxygen species (ROS) in skeletal muscle cells(2011) Cabello Verrugio, Claudio Alejandro; Morales France, María Gabriela; Brandan, Enrique