Person: Pino Sans, Javier Del
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First Name
Javier Del
Last Name
Pino Sans
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Veterinaria
Department
Farmacología y Toxicología
Area
Toxicología
Identifiers
13 results
Search Results
Now showing 1 - 10 of 13
Item Cadmium alters heat shock protein pathways in SN56 cholinergic neurons, leading to AB and phosphorylated Tau protein generation and cell death(Food and Chemical Toxicology, 2018) Moyano-Cires Ivanoff, Paula Viviana; García Sánchez, José Manuel; Lobo Alonso, Margarita; Anadón Baselga, María José; Sola Vendrell, Emma; Pelayo Alarcón, Adela; García Lobo, Jimena; Frejo Moya, María Teresa; Pino Sans, Javier DelCadmium, a neurotoxic environmental compound, produces cognitive disorders, although the mechanism remains unknown. Cadmium induces a more pronounced cell death on cholinergic neurons from basal forebrain (BF), mediated, in part, by increase in Aβ and total and phosphorylated Tau protein levels, which may explain cadmium effects on learning and memory processes. Cadmium downregulates the expression of heat shock proteins (HSPs) HSP 90, HSP70 and HSP27, and of HSF1, the master regulator of the HSP pathway. HSPs proteins reduce the production of Aβ and phosphorylated Tau proteins and avoid cell death pathways induction. Thus, we hypothesized that cadmium induced the production of Aβ and Tau proteins by HSP pathway disruption through HSF1 expression alteration, leading to BF cholinergic neurons cell death. Our results show that cadmium downregulates HSF1, leading to HSP90, HSP70 and HSP27 gene expression downregulation in BF SN56 cholinergic neurons. In addition, cadmium induced Aβ and total and phosphorylated Tau proteins generation, mediated partially by HSP90, HSP70 and HSP27 disruption, leading to cell death. These results provide new understanding of the mechanisms contributing to cadmium harmful effects on cholinergic neurons.Item Insulin Signaling Disruption and INF-γ Upregulation Induce Aβ1–42 and Hyperphosphorylated-Tau Proteins Synthesis and Cell Death after Paraquat Treatment of Primary Hippocampal Cells(Chemical Research in Toxicology, 2022) Abascal, Maria Luisa; Sanjuan, Javier; Moyano-Cires Ivanoff, Paula Viviana; Sola Vendrell, Emma; Flores, Andrea; García Sánchez, José Manuel; García Lobo, Jimena; Frejo Moya, María Teresa; Pino Sans, Javier DelAcute and long-term paraquat (PQ) exposure produces hippocampal neurodegeneration and cognition decline. Although some mechanisms involved in these effects were found, the rest are unknown. PQ treatment, for 1 and 14 days, upregulated interferon-gamma signaling, which reduced insulin levels and downregulated the insulin pathway through phosphorylated-c-Jun N-terminal-kinase upregulation, increasing glucose levels and the production of Aβ1–42 and phosphorylated-tau, by beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) overexpression and phosphorylated-GSK3β (p-GSK3β; ser9) level reduction, respectively, which induced primary hippocampal neuronal loss. This novel information on the PQ mechanisms leading to hippocampal neurodegeneration could help reveal the PQ actions that lead to cognition dysfunction.- Project number: 95
Item Aprendizaje global, flexible y personalizado para atender la diversidad en el aula, mediante el uso de Flipped Learning, a través del uso integrado de un sistema virtual de respuesta en el aula, y otras herramientas TACs digitales(2021) Pino Sans, Javier Del; Moyano-Cires Ivanoff, Paula Viviana; Frejo Moya, María Teresa; Anadón Baselga, María José; Lobo Alonso, Margarita; Pelayo Alarcon, Adela; Capo Marti, Miguel Andrés; Sola Vendrell, Emma; Sanjuán López, Javier; García Sánchez, José Manuel; Ruiz Fernandez, Matilde; Mourin Moral, Francisco Javier; Frias González, Mariano De; Naval López, María Victoria; Guerra Menéndez, Lucia; García Lobo, Jimena Item Manganese induced ROS and AChE variants alteration leads to SN56 basal forebrain cholinergic neuronal loss after acute and long-term treatment(Food and Chemical Toxicology, 2019) Moyano-Cires Ivanoff, Paula Viviana; García Sánchez, José Manuel; Anadón Baselga, María José; Lobo Alonso, Margarita; García Lobo, Jimena; Frejo Moya, María Teresa; Sola Vendrell, Emma; Pelayo Alarcón, Adela; Pino Sans, Javier DelManganese (Mn) induces cognitive disorders and basal forebrain (BF) cholinergic neuronal loss, involved on learning and memory regulation, which could be the cause of such cognitive disorders. However, the mechanisms through which it induces these effects are unknown. We hypothesized that Mn could induce BF cholinergic neuronal loss through oxidative stress generation, cholinergic transmission and AChE variants alteration that could explain Mn cognitive disorders. This study shows that Mn impaired cholinergic transmission in SN56 cholinergic neurons from BF through alteration of AChE and ChAT activity and CHT expression. Moreover, Mn induces, after acute and long-term exposure, AChE variants alteration and oxidative stress generation that leaded to lipid peroxidation and protein oxidation. Finally, Mn induces cell death on SN56 cholinergic neurons and this effect is independent of cholinergic transmission alteration, but was mediated partially by oxidative stress generation and AChE variants alteration. Our results provide new understanding of the mechanisms contributing to the harmful effects of Mn on cholinergic neurons and their possible involvement in cognitive disorders induced by Mn.Item Bisphenol-A Neurotoxic Effects on Basal Forebrain Cholinergic Neurons In Vitro and In Vivo(Biology, 2023) Flores, Andrea; Moyano-Cires Ivanoff, Paula Viviana; Sola Vendrell, Emma; García Sánchez, José Manuel; García Lobo, Jimena; Frejo Moya, María Teresa; Guerra Menéndez, Lucía; Labajo González, Elena; Lobo Lozano, Inés; Abascal, Luisa; Pino Sans, Javier DelThe widely used plasticizer bisphenol-A (BPA) is well-known for producing neurodegeneration and cognitive disorders, following acute and long-term exposure. Although some of the BPA actions involved in these effects have been unraveled, they are still incompletely known. Basal forebrain cholinergic neurons (BFCN) regulate memory and learning processes and their selective loss, as observed in Alzheimer’s disease and other neurodegenerative diseases, leads to cognitive decline. In order to study the BPA neurotoxic effects on BFCN and the mechanisms through which they are induced, 60-day old Wistar rats were used, and a neuroblastoma cholinergic cell line from the basal forebrain (SN56) was used as a basal forebrain cholinergic neuron model. Acute treatment of rats with BPA (40 µg/kg) induced a more pronounced basal forebrain cholinergic neuronal loss. Exposure to BPA, following 1- or 14-days, produced postsynaptic-density-protein-95 (PSD95), synaptophysin, spinophilin, and N-methyl-D-aspartate-receptor-subunit-1 (NMDAR1) synaptic proteins downregulation, an increase in glutamate content through an increase in glutaminase activity, a downregulation in the vesicular-glutamate-transporter-2 (VGLUT2) and in the WNT/β-Catenin pathway, and cell death in SN56 cells. These toxic effects observed in SN56 cells were mediated by overexpression of histone-deacetylase-2 (HDAC2). These results may help to explain the synaptic plasticity, cognitive dysfunction, and neurodegeneration induced by the plasticizer BPA, which could contribute to their prevention.Item Manganese increases Aβ and Tau protein levels through proteasome 20S and heat shock proteins 90 and 70 alteration, leading to SN56 cholinergic cell death following single and repeated treatment(Ecotoxicology and Environmental Safety, 2020) Moyano-Cires Ivanoff, Paula Viviana; García Sánchez, José Manuel; García Lobo, Jimena; Anadón Baselga, María José; Naval López, María Victoria; Frejo Moya, María Teresa; Sola Vendrell, Emma; Pelayo Alarcón, Adela; Pino Sans, Javier DelManganese (Mn) produces cholinergic neuronal loss in basal forebrain (BF) region that was related to cognitive dysfunction induced after single and repeated Mn treatment. All processes that generate cholinergic neuronal loss in BF remain to be understood. Mn exposure may produce the reduction of BF cholinergic neurons by increasing amyloid beta (Aβ) and phosphorylated Tau (pTau) protein levels, altering heat shock proteins’ (HSPs) expression, disrupting proteasome P20S activity and generating oxidative stress. These mechanisms, described to be altered by Mn in regions different than BF, could lead to the memory and learning process alteration produced after Mn exposure. The research performed shows that single and repeated Mn treatment of SN56 cholinergic neurons from BF induces P20S inhibition, increases Aβ and pTau protein levels, produces HSP90 and HSP70 proteins expression alteration, and oxidative stress generation, being the last two effects mediated by NRF2 pathway alteration. The increment of Aβ and pTau protein levels was mediated by HSPs and proteasome dysfunction. All these mechanisms mediated the cell decline observed after Mn treatment. Our results are relevant because they may assist to reveal the processes leading to the neurotoxicity and cognitive alterations observed after Mn exposure.- Project number: 160
Item Aprendizaje flexible y personalizado para atender la diversidad en el aula, mediante la gamificación, a través del uso integrado de un sistema virtual de respuesta en el aula para dispositivos móviles con acceso a internet y una aplicación de screencasting(2018) Pino Sans, Javier Del; Martin Sopeña, Alejandra; López Salas, Alejandra; De Frías González, Mariano; Zeballos Deza, Gabriela; Moyano-Cires Ivanoff, Paula Viviana; García Sánchez, José Manuel; Frejo Moya, María Teresa; Anadón Baselga, María José; Capó Martí, Miguel Andrés; Díaz Plaza, María Jesús; Lobo Alonso, Margarita; García Lobo, Jimena; Pelayo Alarcon, Adela; Blanco Caneda, Maria Luisa; Peligros Gómez, Isabel; Menarguez Palanca, Javier; López Varela, María del Carmen; Medina Ortega, Luis; Rodriguez Gil, Yolanda; Agra Pujol, Carolina; Fernández Aceñero, María Jesús; Sola Vendrell, Emma - Project number: 267
Item Aprendizaje colaborativo/competitivo mediante gamificación, a través del uso integrado de un mando wiimote como pizarra digital interactiva, un sistema virtual de respuesta en el aula, y dispositivos móviles con acceso a internet(2017) Pino Sans, Javier Del; Anadon Baselga, María Jose; Frejo Moya, María Teresa; Diaz Plaza, María Jesús; Capó Martí, Miguel Andrés; García Lobo, Jimena; Lobo Alonso, Margarita; Moyano-Cires Ivanoff, Paula Viviana; Zeballos Deza, Gabriela; Flores Calle, AndreaIntegración de pizarra digital, una aplicación informática propia como sistema de respuesta (clicker) y otras aplicaciones no propias para facilitar la evaluación continua, aumentar la motivación y rendimiento de los estudiantes a un coste muy bajo. - Project number: 164
Item Aprendizaje global, flexible y personalizado para atender la diversidad y la inserción laboral, usando el flipped learning, integrando mundos y sistemas virtuales de respuesta en el aula, y otras herramientas TACs digitales(2022) Moyano-Cires Ivanoff, Paula Viviana; Anadón Baselga, María José; Pino Sans, Javier Del; Frejo Moya, María Teresa; Pelayo Alarcon, Adela; Sola Vendrell, Emma; Naval López, María Victoria; Capo Marti, Miguel Andrés; Guerra Menéndez, Lucia; Flores Calle, Andrea; Ruiz Fernandez, Matilde; García Sánchez, José Manuel; García Lobo, Jimena; Lobo Alonso, Margarita; De Frías González, Mariano; Sanjuán López, Javier; Vílchez Romero, Carmen; Sanz Rey, Laura; Manzano Reyes, Ana María; Bellón López, Miguel Angel - Project number: 14
Item Aprendizaje flexible y personalizado para atender la diversidad en el aula, mediante el uso del flipped learning (aprendizaje invertido), a través del uso integrado de un sistema virtual de respuesta en el aula, y otras herramientas TACs(2020) Pino Sans, Javier Del; Moyano-Cires Ivanoff, Paula Viviana; Frejo Moya, María Teresa; Lobo Alonso, Margarita; García Lobo, Jimena; Anadón Baselga, María José; Capo Marti, Miguel Andrés; Frias González, Mariano De; Rojas López, Francisco Javier; Ruiz Fernández, Matilde; Sola Vendrell, Emma; Mourin Moral, Francisco Javier; Sanjuán López, Javier; García Sánchez, José ManuelIntegración de una aplicación informática propia como sistema de respuesta (clicker) y diferentes herramientas TCs para facilitar la evaluación continua de forma personalizada, aumentar la motivación y rendimiento de los estudiantes a bajo coste.