Browsing by Author "Ríos Leal, Juvenal Antonio"

Now showing 1 - 7 of 7
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    Bases biológicas del cáncer: una propuesta de contenidos mínimos para las carreras de la salud
    (2021) Garrido Cisterna, Francisco Javier; Ríos Leal, Juvenal Antonio; Zavala, Valentina; Zolezzi, Juan; Labbé, Tomás; Roje, Dunja; García Bloj, Benjamín; Barake Sabbagh, M. Francisca; Universidad San Sebastián; University of California, Davis; Universidad de Magallanes; Universidad de Santiago; Fundación Nuestros Hijos; Universidad Mayor
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    Formación científica en el pregrado de medicina en Chile : ¿dónde estamos? y ¿hacia dónde vamos?
    (2020) Garrido Cisterna, Francisco Javier; Labbé Atenas, Tomás; Paris Mancilla, Oscar Enrique; Ríos Leal, Juvenal Antonio
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    Is Alzheimer's disease related to metabolic syndrome? A Wnt signaling conundrum
    (2014) Ríos Leal, Juvenal Antonio; Arrese Jiménez, Marco; Barja Y., Salesa; Inestrosa Cantín, Nibaldo
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    Nicotine Prevents Synaptic Impairment Induced by Amyloid-beta Oligomers Through alpha 7-Nicotinic Acetylcholine Receptor Activation
    (2013) Inestrosa Cantín, Nibaldo; Godoy Zeballos, Juan Alejandro; Vargas, J.; Arrazola, M.; Ríos Leal, Juvenal Antonio; Carvajal, F.; Serrano, F.; Farías, G.
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    Signaling pathway cross talk in Alzheimer's disease
    (2014) Godoy Zeballos, Juan Alejandro; Ríos Leal, Juvenal Antonio; Inestrosa Cantín, Nibaldo
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    Situación actual del cáncer de colon en Chile : Una mirada traslacional
    (2020) Ríos Leal, Juvenal Antonio; Barake Sabbagh, M. Francisca; Arce, M. J.; Francisco, López-Köstner; Labbe, T. P.; Villena, J.; Becerra, S.
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    Wnt3a ligand facilitates autophagy in hippocampal neurons by modulating a novel GSK-3β-AMPK axis
    (2018) Ríos Leal, Juvenal Antonio; Godoy Zeballos, Juan Alejandro; Inestrosa Cantín, Nibaldo
    Abstract Background In the adult central nervous system (CNS), Wnt signaling regulates dendritic structure and synaptic plasticity. The Wnt signaling pathway can be divided into the canonical (β-catenin-dependent) and non-canonical pathways. In the canonical pathway, the binding of canonical ligands such as Wnt3a to the Frizzled receptor induces inactivation of glycogen synthase kinase-3β (GSK-3β), which stabilizes β-catenin and allows its translocation to the nucleus. However, to date, few studies have focused on β-catenin-independent Wnt signaling or explained the underlying mechanisms connecting Wnt signaling to cellular energy metabolism. A recent study demonstrated negative regulation of 5′ adenosine monophosphate-activated protein kinase (AMPK), a major target of GSK-3β that regulates cellular metabolism under diverse conditions. Mainly based on these observations, we evaluated whether Wnt3a ligand modulates autophagy by regulating the GSK-3β/AMPK axis. Methods Cultured primary hippocampal neurons and slices of the CA1 region of rat hippocampus were used. GSK-3β inhibition, AMPK activation, PP2Ac expression, and LC3 processing were examined by western blotting. Autophagic compartments were studied using the CYTO-ID® fluorescent probe, and mature autophagosomes were observed via transmission electron microscopy (TEM). Results Wnt3a ligand, acting through the Frizzled receptor, promotes the rapid activation of AMPK by inactivating GSK-3β. Biochemical analysis of downstream targets indicated that Wnt3a ligand modulates autophagy in hippocampal neurons. Conclusions Our results revealed new aspects of Wnt signaling in neuronal metabolism. First, AMPK is an additional target downstream of the Wnt cascade, suggesting a molecular mechanism for the metabolic effects previously observed for Wnt signaling. Second, this mechanism is independent of β-catenin, suggesting a relevant role for non-genomic activity of the Wnt pathway in cellular metabolism. Finally, these results have new implications regarding the role of Wnt signaling in the modulation of autophagy in neurons, with a possible role in the removal of accumulated intracellular proteins.Abstract Background In the adult central nervous system (CNS), Wnt signaling regulates dendritic structure and synaptic plasticity. The Wnt signaling pathway can be divided into the canonical (β-catenin-dependent) and non-canonical pathways. In the canonical pathway, the binding of canonical ligands such as Wnt3a to the Frizzled receptor induces inactivation of glycogen synthase kinase-3β (GSK-3β), which stabilizes β-catenin and allows its translocation to the nucleus. However, to date, few studies have focused on β-catenin-independent Wnt signaling or explained the underlying mechanisms connecting Wnt signaling to cellular energy metabolism. A recent study demonstrated negative regulation of 5′ adenosine monophosphate-activated protein kinase (AMPK), a major target of GSK-3β that regulates cellular metabolism under diverse conditions. Mainly based on these observations, we evaluated whether Wnt3a ligand modulates autophagy by regulating the GSK-3β/AMPK axis. Methods Cultured primary hippocampal neurons and slices of the CA1 region of rat hippocampus were used. GSK-3β inhibition, AMPK activation, PP2Ac expression, and LC3 processing were examined by western blotting. Autophagic compartments were studied using the CYTO-ID® fluorescent probe, and mature autophagosomes were observed via transmission electron microscopy (TEM). Results Wnt3a ligand, acting through the Frizzled receptor, promotes the rapid activation of AMPK by inactivating GSK-3β. Biochemical analysis of downstream targets indicated that Wnt3a ligand modulates autophagy in hippocampal neurons. Conclusions Our results revealed new aspects of Wnt signaling in neuronal metabolism. First, AMPK is an additional target downstream of the Wnt cascade, suggesting a molecular mechanism for the metabolic effects previously observed for Wnt signaling. Second, this mechanism is independent of β-catenin, suggesting a relevant role for non-genomic activity of the Wnt pathway in cellular metabolism. Finally, these results have new implications regarding the role of Wnt signaling in the modulation of autophagy in neurons, with a possible role in the removal of accumulated intracellular proteins.Abstract Background In the adult central nervous system (CNS), Wnt signaling regulates dendritic structure and synaptic plasticity. The Wnt signaling pathway can be divided into the canonical (β-catenin-dependent) and non-canonical pathways. In the canonical pathway, the binding of canonical ligands such as Wnt3a to the Frizzled receptor induces inactivation of glycogen synthase kinase-3β (GSK-3β), which stabilizes β-catenin and allows its translocation to the nucleus. However, to date, few studies have focused on β-catenin-independent Wnt signaling or explained the underlying mechanisms connecting Wnt signaling to cellular energy metabolism. A recent study demonstrated negative regulation of 5′ adenosine monophosphate-activated protein kinase (AMPK), a major target of GSK-3β that regulates cellular metabolism under diverse conditions. Mainly based on these observations, we evaluated whether Wnt3a ligand modulates autophagy by regulating the GSK-3β/AMPK axis. Methods Cultured primary hippocampal neurons and slices of the CA1 region of rat hippocampus were used. GSK-3β inhibition, AMPK activation, PP2Ac expression, and LC3 processing were examined by western blotting. Autophagic compartments were studied using the CYTO-ID® fluorescent probe, and mature autophagosomes were observed via transmission electron microscopy (TEM). Results Wnt3a ligand, acting through the Frizzled receptor, promotes the rapid activation of AMPK by inactivating GSK-3β. Biochemical analysis of downstream targets indicated that Wnt3a ligand modulates autophagy in hippocampal neurons. Conclusions Our results revealed new aspects of Wnt signaling in neuronal metabolism. First, AMPK is an additional target downstream of the Wnt cascade, suggesting a molecular mechanism for the metabolic effects previously observed for Wnt signaling. Second, this mechanism is independent of β-catenin, suggesting a relevant role for non-genomic activity of the Wnt pathway in cellular metabolism. Finally, these results have new implications regarding the role of Wnt signaling in the modulation of autophagy in neurons, with a possible role in the removal of accumulated intracellular proteins.