Browsing by Author "Morales France, María Gabriela"
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- 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
- 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
- ItemDeficiency of Niemann-Pick C1 protein protects against diet-induced gallstone formation in mice(2010) Morales France, María Gabriela; Amigo Böker, Ludwig Peter; Balboa Castillo, Elisa Ivana; Acuña Aravena, Mariana Loreto; Castro, Juan; Molina, Héctor; Miquel P., Juan Francisco; Nervi, Flavio; Rigotti Rivera, Attilio; Zanlungo Matsuhiro, Silvana
- 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
- ItemNovel and optimized strategies for inducing fibrosis in vivo: Focus on Duchenne Muscular Dystrophy(2014) Pessina, P.; Cabrera García, Daniel Alejandro; Morales France, María Gabriela; Riquelme Illanes, Cecilia Angélica
- ItemNpc1 deficiency in the C57BL/6J genetic background enhances Niemann–Pick disease type C spleen pathology(2011) Parra Cares, Julio Alejandro; Klein, Andres D.; Castro, Juan Francisco; Morales France, María Gabriela; Mosqueira Montero, Matías José; Valencia Araya, Ilse; Cortés Mora, Víctor Antonio; Rigotti Rivera, Attilio; Zanlungo Matsuhiro, SilvanaNiemann–Pick type C (NPC) disease is an autosomal recessive neurovisceral lipid storage disorder. The affected genes are NPC1 and NPC2. Mutations in either gene lead to intracellular cholesterol accumulation. There are three forms of the disease, which are categorized based on the onset and severity of the disease: the infantile form, in which the liver and spleen are severely affected, the juvenile form, in which the liver and brain are affected, and the adult form, which affects the brain. In mice, a spontaneous mutation in the Npc1 gene originated in the BALB/c inbred strain mimics the juvenile form of the disease. To study the influence of genetic background on the expression of NPC disease in mice, we transferred the Npc1 mutation from the BALB/c to C57BL/6J inbred background. We found that C57BL/6J-Npc1−/− mice present with a much more aggressive form of the disease, including a shorter lifespan than BALB/c-Npc1−/− mice. Surprisingly, there was no difference in the amount of cholesterol in the brains of Npc1−/− mice of either mouse strain. However, Npc1−/− mice with the C57BL/6J genetic background showed striking spleen damage with a marked buildup of cholesterol and phospholipids at an early age, which correlated with large foamy cell clusters. In addition, C57BL/6J Npc1−/− mice presented red cell abnormalities and abundant ghost erythrocytes that correlated with a lower hemoglobin concentration. We also found abnormalities in white cells, such as cytoplasmic granulation and neutrophil hypersegmentation that included lymphopenia and atypias. In conclusion, Npc1 deficiency in the C57BL6/J background is associated with spleen, erythrocyte, and immune system abnormalities that lead to a reduced lifespan.
- ItemReducing CTGF/CCN2 slows down mdx muscle dystrophy and improves cell therapy(2013) Morales France, María Gabriela; Gutiérrez Pérez, Jaime Agustín; Cabello Verrugio, Claudio Alejandro; Cabrera, Daniel; Lipson, Kenneth E.; Goldschmeding, Roel; Brandan, Enrique