Person:
Pérez Díaz, Carmen

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First Name
Carmen
Last Name
Pérez Díaz
URI
https://hdl.handle.net/20.500.14352/80544
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Veterinaria
Department
Medicina y Cirugía Animal
Area
Medicina y Cirugía Animal
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2016 - 20184
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End date: 2018 × Start date: 2016 ×

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Now showing 1 - 4 of 4
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    Up-regulation of CB2 receptors in reactive astrocytes in canine degenerative myelopathy, a disease model of amyotrophic lateral sclerosis
    (Disease Models Mechanisms, 2017) Fernández-Trapero, María; Coates, Joan R.; Rodríguez Cueto, Carmen Aurora; Lago Femia, Eva De; Pérez Díaz, Carmen; Fernández Ruiz, José Javier; Espejo Porras, Francisco
    Targeting of the CB2 receptor results in neuroprotection in the SOD1G93A mutant mouse model of amyotrophic lateral sclerosis (ALS). The neuroprotective effects of CB2 receptors are facilitated by their upregulation in the spinal cord of the mutant mice. Here, we investigated whether similar CB2 receptor upregulation, as well as parallel changes in other endocannabinoid elements, is evident in the spinal cord of dogs with degenerative myelopathy (DM), caused by mutations in the superoxide dismutase 1 gene (SOD1). We used well-characterized post-mortem spinal cords from unaffected and DM-affected dogs. Tissues were used first to confirm the loss of motor neurons using Nissl staining, which was accompanied by glial reactivity (elevated GFAP and Iba-1 immunoreactivity). Next, we investigated possible differences in the expression of endocannabinoid genes measured by qPCR between DM-affected and control dogs. We found no changes in expression of the CB1 receptor (confirmed with CB1 receptor immunostaining) or NAPE-PLD, DAGL, FAAH and MAGL enzymes. In contrast, CB2 receptor levels were significantly elevated in DM-affected dogs determined by qPCR and western blotting, which was confirmed in the grey matter using CB2 receptor immunostaining. Using double-labelling immunofluorescence, CB2 receptor immunolabelling colocalized with GFAP but not Iba-1, indicating upregulation of CB2 receptors on astrocytes in DM-affected dogs. Our results demonstrate a marked upregulation of CB2 receptors in the spinal cord in canine DM, which is concentrated in activated astrocytes. Such receptors could be used as a potential target to enhance the neuroprotective effects exerted by these glial cells.
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    Project number: 119
    Virtualización e impresión 3D de modelos anatómicos aplicados a la docencia y planificación quirúrgica
    (2017) Pérez Díaz, Carmen; Rojo Salvador, Concepción; Gaspar Simón, Ignacio de; Sanz Dueñas, Javier; Rodríguez Quirós, Jesús; López Rodriguez, Juan; Barroso Santos-Carvalho, Paulo; Llorca Martín, Celia; Crenes Vazquez, Maria Eugenia; Perianes Rodriguez, Iñigo; Portero Fuentes, Miriam; Paton Rubio, David
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    Neurodevelopmental alterations and seizures developed by mouse model of infantile hypophosphatasia are associated with purinergic signalling deregulation
    (Human Molecular Genetics, 2016) Sebastián Serrano, Álvaro; Engel, Tobias; De Diego García, Laura; Olivos Ore, Luis Alcides; Arribas Blázquez, Marina; Martínez-Frailes, Carlos; Pérez Díaz, Carmen; Millán, José Luis ; Miras Portugal, María Teresa; Rodríguez Artalejo, Antonio; Henshall, David; Díaz Hernández, Miguel
    Hypomorphic mutations in the gene encoding the tissue-nonspecific alkaline phosphatase (TNAP) enzyme, ALPL in human or Akp2 in mice, cause hypophosphatasia (HPP), an inherited metabolic bone disease also characterized by spontaneous seizures. Initially, these seizures were attributed to the impairment of GABAergic neurotransmission caused by altered vitamin B6 (vit-B6) metabolism. However, clinical cases in human newborns and adults whose convulsions are refractory to pro-GABAergic drugs but controlled by the vit-B6 administration, suggest that other factors are involved. Here, to evaluate whether neurodevelopmental alterations are underlying the seizures associated to HPP, we performed morphological and functional characterization of postnatal homozygous TNAP null mice, a model of HPP. These analyses revealed that TNAP deficient mice present an increased proliferation of neural precursors, an altered neuronal morphology, and an augmented neuronal activity. We found that these alterations were associated with a partial downregulation of the purinergic P2X7 receptor (P2X7R). Even though deficient P2X7R mice present similar neurodevelopmental alterations, they do not develop neonatal seizures. Accordingly, we found that the additional blockage of P2X7R prevent convulsions and extend the lifespan of mice lacking TNAP. In agreement with these findings, we also found that exogenous administration of ATP or TNAP antagonists induced seizures in adult wild-type mice by activating P2X7R. Finally, our results also indicate that the anticonvulsive effects attributed to vit-B6 may be due to its capacity to block P2X7R. Altogether, these findings suggest that the purinergic signalling regulates the neurodevelopmental alteration and the neonatal seizures associated to HPP.
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    Project number: 123
    Virtualización e impresión 3D de modelos anatómicos aplicados a la docencia en anatomia y cirugía veterinaria II
    (2018) De Gaspar Simón, Ignacio; Rojo Salvador, Concepción; Pérez Díaz, Carmen; Sanz Dueñas, Javier; Sánchez González, Paula; Llorca Martín, Celia; Crenes Vázquez, María Eugenia; Pintado Laguna, Carlota Soledad; Labrador Pérez, Ángela; Rodríguez Quirós, Jesús; De La Morena García, Eva; Villalonga Rodríguez, Luis; Barroso Santos-Carvalho, Paulo; Portero Fuentes, Miriam
    Este proyecto aplica las técnicas de virtualización de imágenes de piezas anatómicas normales y patológicas con fines de creación de modelos digitales y con impresión 3D para docencia en Anatomía y Cirugía Veterinarias.