Browsing by Author "Metz Baer, Claudia Andrea"

Now showing 1 - 11 of 11
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    Anti-Ribosomal P Protein Autoantibodies From Patients With Neuropsychiatric Lupus Impair Memory in Mice
    (2015) Bravo Zehnder, Marcela; Toledo, Enrique M.; Segovia Miranda, Fabian; Serrano, Felipe G.; Benito, Maria J.; Metz Baer, Claudia Andrea; Retamal, Claudio; Álvarez Rojas, Alejandra; Massardo Vega, Loreto; Inestrosa Cantín, Nibaldo
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    Epidermal growth factor receptor endocytic traffic perturbation by phosphatidate phosphohydrolase inhibition : new strategy against cancer
    (2014) Shaughnessy, Ronan Patrick; Retamal, Claudio; Oyanadel, Claudia; Norambuena Pérez, Andrés; López, Alejandro; Bravo Zehnder, Marcela; Montecino, Fabián, J.; Metz Baer, Claudia Andrea; Soza Gajardo, Andrea; González de la Rosa, Alfonso
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    Galectin-8 binds to LFA-1, blocks its interaction with ICAM-1 and is counteracted by anti-Gal-8 autoantibodies isolated from lupus patients
    (2013) Vicuña, Lucas; Pardo, Evelyn; Curkovic, Cristóbal; Doger, Remziye; Oyanadel, Claudia; Metz Baer, Claudia Andrea; Massardo Vega, Loreto; González de la Rosa, Alfonso; Soza Gajardo, Andrea
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    Galectin-8 induces partial epithelial–mesenchymal transition with invasive tumorigenic capabilities involving a FAK/EGFR/proteasome pathway in Madin–Darby canine kidney cells
    (2018) Oyanadel, Claudia; Holmes Videla, Christopher Edward; Pardo Huguet, Evelyn Cristina; Retamal Villarroel, Claudio Enrique; Shaughnessy, Ronan Patrick; Smith, Patricio C.; Cortés Martínez, Priscilla Rocío; Bravo Zehnder, Marcela; Metz Baer, Claudia Andrea; Feuerhake, Teo; Romero, Diego; Roa Strauch, Juan Carlos Enrique; Montecinos, Viviana; Soza Gajardo, Andrea; González, Alfonso
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    GALECTIN-8 Is a Neuroprotective Factor in the Brain that Can Be Neutralized by Human Autoantibodies
    (2019) Pardo Huguet, Evelyn Cristina; Barake Sabbagh, M. Francisca; Godoy Zeballos, Juan Alejandro; Oyanadel, C.; Espinoza, S.; Metz Baer, Claudia Andrea; Retamal, C.; Massardo Vega, Loreto; Tapia-Rojas, Cheril; Inestrosa Cantín, Nibaldo; Soza, Alejandro; Gonzalez, A.
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    Galectin-8 mediates fibrogenesis induced by cyclosporine in human gingival fibroblasts
    (2020) Patricio C. Smith; Metz Baer, Claudia Andrea; Peña, Adely de la; Oyanadel, Claudia; Ávila, Patricio; Arancibia, Rodrigo; Vicuña, Lucas; Retamal Villarroel, Claudio Enrique; Barake Sabbagh, M. Francisca; González de la Rosa, Alfonso; Soza Gajardo, Andrea
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    Galectin-8 promotes migration and proliferation and prevents apoptosis in U87 glioblastoma cells
    (2016) Metz Baer, Claudia Andrea; Döger, Remziye.; Riquelme Barrientos, Elizabeth Carolina.; Cortés Martínez, Priscilla Rocío; Holmes Videla, Christopher Edward; Shaughnessy, Ronan.; Oyanadel, Claudia.; Grabowski Pinto, Catalina.; González de la Rosa, Alfonso; Soza Gajardo, Andrea
    Abstract Background Glioblastoma is one of the most aggressive cancers of the brain. Malignant traits of glioblastoma cells include elevated migration, proliferation and survival capabilities. Galectins are unconventionally secreted glycan-binding proteins that modulate processes of cell adhesion, migration, proliferation and apoptosis by interacting with beta-galactosides of cell surface glycoproteins and the extracellular matrix. Galectin-8 is one of the galectins highly expressed in glioblastoma cells. It has a unique selectivity for terminally sialylated glycans recently found enhanced in these highly malignant cells. A previous study in glioblastoma cell lines reported that Gal-8 coating a plastic surface stimulates two-dimensional motility. Because in other cells Gal-8 arrests proliferation and induces apoptosis, here we extend its study by analyzing all of these processes in a U87 glioblastoma cell model. Methods We used immunoblot and RT-PCR for Gal-8 expression analysis, recombinant Gal-8 produced in a bacteria system for Gal-8 treatment of the cells, and shRNA in lentivirus transduction for Gal-8 silencing. Cell migration as assessed in transwell filters. Cell proliferation, cell cycle and apoptosis were analyzed by FACS. Results Gal-8 as a soluble stimulus triggered chemotactic migration of U87 cells across the polycarbonate filter of transwell chambers, almost as intensively as fetal bovine serum. Unexpectedly, Gal-8 also enhanced U87 cell growth. Co-incubation of Gal-8 with lactose, which blocks galectin–glycan interactions, abrogated both effects. Immunoblot showed Gal-8 in conditioned media reflecting its secretion. U87 cells transduced with silencing shRNA in a lentiviral vector expressed and secreted 30–40 % of their normal Gal-8 levels. These cells maintained their migratory capabilities, but decreased their proliferation rate and underwent higher levels of apoptosis, as revealed by flow cytometry analysis of cell cycle, CFSE and activated caspase-3 staining. Proliferation seemed to be more sensitive than migration to Gal-8 expression levels. Conclusions Gal-8, either secreted or exogenously enriched in the media, and acting through extracellular glycan interactions, constitutes a strong stimulus of directional migration in glioblastoma U87 cells and for the first time emerges as a factor that promotes proliferation and prevents apoptosis in cancerous cells. These properties could potentially contribute to the exaggerated malignancy of glioblastoma cells.Abstract Background Glioblastoma is one of the most aggressive cancers of the brain. Malignant traits of glioblastoma cells include elevated migration, proliferation and survival capabilities. Galectins are unconventionally secreted glycan-binding proteins that modulate processes of cell adhesion, migration, proliferation and apoptosis by interacting with beta-galactosides of cell surface glycoproteins and the extracellular matrix. Galectin-8 is one of the galectins highly expressed in glioblastoma cells. It has a unique selectivity for terminally sialylated glycans recently found enhanced in these highly malignant cells. A previous study in glioblastoma cell lines reported that Gal-8 coating a plastic surface stimulates two-dimensional motility. Because in other cells Gal-8 arrests proliferation and induces apoptosis, here we extend its study by analyzing all of these processes in a U87 glioblastoma cell model. Methods We used immunoblot and RT-PCR for Gal-8 expression analysis, recombinant Gal-8 produced in a bacteria system for Gal-8 treatment of the cells, and shRNA in lentivirus transduction for Gal-8 silencing. Cell migration as assessed in transwell filters. Cell proliferation, cell cycle and apoptosis were analyzed by FACS. Results Gal-8 as a soluble stimulus triggered chemotactic migration of U87 cells across the polycarbonate filter of transwell chambers, almost as intensively as fetal bovine serum. Unexpectedly, Gal-8 also enhanced U87 cell growth. Co-incubation of Gal-8 with lactose, which blocks galectin–glycan interactions, abrogated both effects. Immunoblot showed Gal-8 in conditioned media reflecting its secretion. U87 cells transduced with silencing shRNA in a lentiviral vector expressed and secreted 30–40 % of their normal Gal-8 levels. These cells maintained their migratory capabilities, but decreased their proliferation rate and underwent higher levels of apoptosis, as revealed by flow cytometry analysis of cell cycle, CFSE and activated caspase-3 staining. Proliferation seemed to be more sensitive than migration to Gal-8 expression levels. Conclusions Gal-8, either secreted or exogenously enriched in the media, and acting through extracellular glycan interactions, constitutes a strong stimulus of directional migration in glioblastoma U87 cells and for the first time emerges as a factor that promotes proliferation and prevents apoptosis in cancerous cells. These properties could potentially contribute to the exaggerated malignancy of glioblastoma cells.
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    Scavenger receptor-A deficiency impairs immune response of microglia and astrocytes potentiating alzheimer's disease pathophysiology
    (2018) Cornejo Castillo, Francisca Alejandra; Vruwink, Marianne; Metz Baer, Claudia Andrea; Muñoz, Paola; Salgado Cortés, Nicole Andrea; Poblete, Joaquín; Andrés Coke, María Estela; Eugenín, Jaime; Bernhardi Montgomery, Rommy von