Browsing by Author "Pena-Oyarzun, Daniel"

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    Autophagy and oxidative stress in non-communicable diseases: A matter of the inflammatory state?
    (2018) Pena-Oyarzun, Daniel; Bravo-Sagua, Roberto; Diaz-Vega, Alexis; Aleman, Larissa; Chiong, Mario; Garcia, Lorena; Bambs S., Claudia; Troncoso, Rodrigo; Cifuentes, Mariana; Morselli, Eugenia; Ferreccio Readi, Catterina; Quest, Andrew F. G.; Criollo, Alfred
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    Expression profile of components of the β-catenin destruction complex in oral dysplasia and oral cancer
    (2021) Goni, Francisca J.; Pena-Oyarzun, Daniel; Torres, Vicente A.; Reyes, Montserrat
    Background: Oral cancer represents the sixth most common cancer in the world and is associated with 40-50% survival at 5 years. Within oral malignancies, oral squamous cell carcinoma (OSCC) is commonly preceded by potentially malignant lesions, which, according to histopathological criteria, are referred to as oral dysplasia and their diagnosis are associated with higher rates of malignant transformation towards cancer. We recently reported that aberrant activation of the Wnt/beta catenin pathway is due to overexpression of Wnt ligands in oral dysplasia. However, the expression of other regulators of this pathway, namely components of the beta-catenin destruction complex has not been explored in oral dysplasia.
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    Inhibition of PORCN Blocks Wnt Signaling to Attenuate Progression of Oral Carcinogenesis
    (2024) Pena-Oyarzun, Daniel; Flores, Tania; Torres, Vicente A.; Quest, Andrew F. G.; Lobos-Gonzalez, Lorena; Kretschmar, Catalina; Contreras, Pamela; Maturana-Ramirez, Andrea; Criollo, Alfredo; Reyes, Montserrat
    Purpose: Oral squamous cell carcinoma (OSCC) is commonly preceded by potentially malignant lesions, referred to as oral dysplasia. We recently reported that oral dysplasia is associated with aberrant activation of the Wnt/beta-catenin pathway, due to overexpression of Wnt ligands in a Porcupine (PORCN)-dependent manner. Pharmacologic inhibition of PORCN precludes Wnt secretion and has been proposed as a potential therapeutic approach to treat established cancers. Nevertheless, there are no studies that explore the effects of PORCN inhibition at the different stages of oral carcinogenesis.
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    Integrating the effects of sucrose intake on the brain and white adipose tissue: Could autophagy be a possible link?
    (WILEY, 2022) Mattar, Pamela; Toledo-Valenzuela, Lilian; Paz Hernandez-Caceres, María; Pena-Oyarzun, Daniel; Morselli, Eugenia; Perez Leighton Claudio Esteban
    Excess dietary sucrose is associated with obesity and metabolic diseases. This relationship is driven by the malfunction of several cell types and tissues critical for the regulation of energy balance, including hypothalamic neurons and white adipose tissue (WAT). However, the mechanisms behind these effects of dietary sucrose are still unclear and might be independent of increased adiposity. Accumulating evidence has indicated that dysregulation of autophagy, a fundamental process for maintenance of cellular homeostasis, alters energy metabolism in hypothalamic neurons and WAT, but whether autophagy could mediate the detrimental effects of dietary sucrose on hypothalamic neurons and WAT that contribute to weight gain is a matter of debate. In this review, we examine the hypothesis that dysregulated autophagy in hypothalamic neurons and WAT is an adiposity-independent effect of sucrose that contributes to increased body weight gain. We propose that excess dietary sucrose leads to autophagy unbalance in hypothalamic neurons and WAT, which increases caloric intake and body weight, favoring the emergence of obesity and metabolic diseases.
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    Polycystin-2 Is Required for Starvation- and Rapamycin-Induced Atrophy in Myotubes
    (2019) Kretschmar, Catalina; Pena-Oyarzun, Daniel; Hernando, Cecilia; Hernandez-Moya, Nadia; Molina-Berrios, Alfredo; Paz Hernandez-Caceres, Maria; Lavandero, Sergio; Budini, Mauricio; Morselli, Eugenia; Parra, Valentina; Troncoso, Rodrigo; Criollo, Alfredo
    Muscle atrophy involves a massive catabolism of intracellular components leading to a significant reduction in cellular and tissue volume. In this regard, autophagy, an intracellular mechanism that degrades proteins and organelles, has been implicated with muscle breakdown. Recently, it has shown that polycystin-2 (PC2), a membrane protein that belongs to the transient receptor potential (TRP) family, is required for the maintenance of cellular proteostasis, by regulating autophagy in several cell types. The role of PC2 in the control of atrophy and autophagy in skeletal muscle remains unknown. Here, we show that PC2 is required for the induction of atrophy in C2C12 myotubes caused by nutrient deprivation or rapamycin exposure. Consistently, overexpression of PC2 induces atrophy in C2C12 myotubes as indicated by decreasing of the myogenic proteins myogenin and caveolin-3. In addition, we show that inhibition of mTORC1, by starvation or rapamycin is inhibited in cells when PC2 is silenced. Importantly, even if PC2 regulates mTORC1, our results show that the regulation of atrophy by PC2 is independent of autophagy. This study provides novel evidence regarding the role of PC2 in skeletal muscle cell atrophy.