Examinando por Autor "Valero-Breton, Mayalen"

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  • Miniatura
    Ítem
    CCL5 Induces a Sarcopenic-like Phenotype via the CCR5 Receptor
    (MDPI, 2025-01-13) Aguirre, Francisco; Tacchi, Franco; Valero-Breton, Mayalen; Orozco-Aguilar, Josué; Conejeros-Lillo, Sanabria; Bonicioli, Josefa; Iturriaga-Jofré, Renata; Cabrera, Daniel; Soto, Jorge A.; Castro-Sepúlveda, Mauricio; Portal-Rodríguez, Marianny; Elorza, ÁLvaro A.; Matamoros, Andrea; Simon, Felipe; Cabello-Verrugio, Claudio
    Sarcopenia corresponds to a decrease in muscle mass and strength. CCL5 is a new myokine whose expression, along with the CCR5 receptor, is increased in sarcopenic muscle. Therefore, we evaluated whether CCL5 and CCR5 induce a sarcopenic-like effect on skeletal muscle tissue and cultured muscle cells. Electroporation in the tibialis anterior (TA) muscle of mice was used to overexpress CCL5. The TA muscles were analyzed by measuring the fiber diameter, the content of sarcomeric proteins, and the gene expression of E3-ligases. C2C12 myotubes and single-isolated flexor digitorum brevis (FDB) fibers were also treated with recombinant CCL5 (rCCL5). The participation of CCR5 was evaluated using the antagonist maraviroc (MVC). Protein and structural analyses were performed. The results showed that TA overexpression of CCL5 led to sarcopenia by reducing muscle strength and mass, muscle-fiber diameter, and sarcomeric protein content, and by upregulating E3-ligases. The same sarcopenic phenotype was observed in myotubes and FDB fibers. We showed increased reactive oxygen species (ROS) production and carbonylated proteins, denoting oxidative stress induced by CCL5. When the CCR5 was antagonized, the effects produced by rCCL5 were prevented. In conclusion, we report for the first time that CCL5 is a novel myokine that exerts a sarcopenic-like effect through the CCR5 receptor.
  • Miniatura
    Ítem
    Severe COVID-19 correlates with lower mitochondrial cristae density in PBMCs and greater sitting time in humans
    (Wiley; The Physiological Society and the American Physiological Society, 2022-05-27) Castro-Sepúlveda, Mauricio; Tapia, German; Tuñón-Suárez, Mauro; Marambio, Hugo; Valero-Breton, Mayalen; Fernández-Verdejo, Rodrigo; Zbinden-Foncea, Hermann
    An interaction between mitochondrial dynamics, physical activity levels, andCOVID-19 severity has been previously hypothesized. However, this has notbeen tested. We aimed to compare mitochondrial morphology and cristae den-sity of PBMCs between subjects with non- severe COVID- 19, subjects with se-vere COVID- 19, and healthy controls. Additionally, we compared the level ofmoderate-vigorous physical activity (MVPA) and sitting time between groups.Blood samples were taken to obtain PBMCs. Mitochondrial dynamics were as-sessed by electron microscopy images and western blot of protein that regulatemitochondrial dynamics. The International Physical Activity Questionnaire(IPAQ; short version) was used to estimate the level of MVPA and the sitting timeThe patients who develop severe COVID-19 (COVID-19++) not present altera-tions of mitochondrial size neither mitochondrial density in comparison to non-severe patients COVID- 19 (COVID- 19) and control subjects (CTRL). However,compared to CTRL, COVID- 19 and COVID-19++ groups have lower mitochon-drial cristae length, a higher proportion of abnormal mitochondrial cristae. TheCOVID-19++ group has lower number (trend) and length of mitochondrial cris-tae in comparison to COVID- 19 group. COVID- 19, but not COVID- 19++ grouphad lower Opa 1, Mfn 2 and SDHB (Complex II) proteins than CTRL group.Besides, COVID-19++ group has a higher time sitting. Our results show that lowmitochondrial cristae density, potentially due to physical inactivity, is associatedwith COVID-19 severity.