Examinando por Autor "Reyes, Ariel E."

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    Cxcl8b and Cxcr2 Regulate Neutrophil Migration through Bloodstream in Zebrafish
    (Hindawi Limited, 2017) Zuñiga-Traslaviña, Constanza; Bravo, Karina; Reyes, Ariel E.; Feijóo, Carmen G.
    Neutrophils play an essential role during an inflammatory response, which is dependent on their rapid recruitment from the bone marrow to the vasculature. However, there is no information about the molecular signals that regulate neutrophil entry to circulation during an inflammatory process in humans. This is mainly due to the lack of a suitable model of study that contains similar set of molecules and that allows in vivo analyses. In this study, we used the zebrafish to assess the role of Cxcl8a, Cxcl8b, and Cxcr2 in neutrophil migration to blood circulation after injury. Using Tg(BACmpx:GFP)i114 transgenic embryos and two damage models (severe and mild), we developed in vivo lack of function assays. We found that the transcription levels of cxcl8a, cxcl8b, and cxcr2 were upregulated in the severe damage model. In contrast, only cxcr2 and cxcl8a mRNA levels were increased during mild damage. After knocking down Cxcl8a, neutrophil quantity decreased at the injury site, while Cxcl8b decreased neutrophils in circulation. When inhibiting Cxcr2, we observed a decrease in neutrophil entry to the bloodstream. In conclusion, we identified different functions for both Cxcl8 paralogues, being the Cxcl8b/Cxcr2 axis that regulates neutrophil entry to the bloodstream, while Cxcl8a/Cxcr2 regulates the migration to the affected area. © 2017 Constanza Zuñiga-Traslaviña et al.
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    Interacción funcional entre histona desacetilasa 9b (hdac9b) y Hilf-1α en la cardiogénesis del pez cebra
    (Universidad Andrés Bello, 2012) Ulloa Valenzuela, Juan Alberto; Reyes, Ariel E.; Bittner O., Mauricio
    A partir de los resultados obtenidos y en relación a la hipótesis planteada, se puede concluir que: 1-Se ha identificado y caracterizado la expresión del transcrito de una HDAC de Clase II en el pez cebra, Hdac9b, que presenta actividad desacetilasa. 2-Se describe por primera vez que Hdac9b participa en el desarrollo del corazón de pez cebra, manteniendo a las CPCs en un estado indiferenciado, regulando de manera negativa la expresión de genes de diferenciación cardiacos. 3-La falta de función de Hdac9b regula la temporalidad de la expresión de los genes de compromiso cardiaco, aumentando su período de expresión. 4-El factor de transcripción candidato que participaría en la extensión del estado indiferenciado de las CPCs es Hif-1 a. 5-Para confirmar la posible interacción entre Hdac9b y Hif-la, sería necesario realizar experimentos de inmunoprecipitación de cromatina.
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    Neutrophil migration in the activation of the innate immune response to different Flavobacterium psychrophilum vaccines in zebrafish (Danio rerio)
    (Hindawi Publishing Corporation, 2015-02) Solís, Camila J.; Poblete-Morales, Matías; Cabral, Sergio; Valdés, Juan A.; Reyes, Ariel E.; Avendaño-Herrera, Ruben; Feijóo, Carmen G.
    Flavobacterium psychrophilum is a Gram-negative bacterium, responsible for the bacterial cold-water disease and the rainbow trout fry syndrome in freshwater salmonid fish. At present, there is only one commercial vaccine in Chile, made with two Chilean F. psychrophilum isolates and another licensed in Europe. The present study analyzed neutrophil migration, as a marker of innate immune activation, in zebrafish (Danio rerio) in response to different F. psychrophilum bath vaccines, which is the first step in evaluating vaccine effectiveness and efficiency in fish. Results indicated that bacterins of the LM-02-Fp isolate were more immunogenic than those from the LM-13-Fp isolate. However, no differences were observed between the same bacteria inactivated by either formaldehyde or heat. Importantly, the same vaccine formulation without an adjuvant only triggered a mild neutrophil migration compared to the complete vaccine. Observations also found that, after a year of storage at 4°C, the activation of the innate immune system by the different vaccines was considerably decreased. Finally, new vaccine formulations prepared with heat and formaldehyde inactivated LM-02-Fp were significantly more efficient than the available commercial vaccine in regard to stimulating the innate immune system. © 2015 Camila J. Solís et al.
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    Overrepresentation of glutamate signaling in alzheimer's disease: Network-based pathway enrichment using meta-analysis of genome-wide association studies
    (Public Library of Science, 2014-04) Pérez-Palma, Eduardo; Bustos, Bernabé I.; Villamán, Camilo F.; Alarcón, Marcelo A.; Avila, Miguel E.; Ugarte, Giorgia D.; Reyes, Ariel E.; Opazo, Carlos; De Ferrari, Giancarlo V.
    Genome-wide association studies (GWAS) have successfully identified several risk loci for Alzheimer’s disease (AD). Nonetheless, these loci do not explain the entire susceptibility of the disease, suggesting that other genetic contributions remain to be identified. Here, we performed a meta-analysis combining data of 4,569 individuals (2,540 cases and 2,029 healthy controls) derived from three publicly available GWAS in AD and replicated a broad genomic region (.248,000 bp) associated with the disease near the APOE/TOMM40 locus in chromosome 19. To detect minor effect size contributions that could help to explain the remaining genetic risk, we conducted network-based pathway analyses either by extracting gene wise p-values (GW), defined as the single strongest association signal within a gene, or calculated a more stringent gene based association p-value using the extended Simes (GATES) procedure. Comparison of these strategies revealed that ontological sub-networks (SNs) involved in glutamate signaling were significantly overrepresented in AD (p,2.7610211, p, 1.9610211; GW and GATES, respectively). Notably, glutamate signaling SNs were also found to be significantly overrepresented (p,5.161028 ) in the Alzheimer’s disease Neuroimaging Initiative (ADNI) study, which was used as a targeted replication sample. Interestingly, components of the glutamate signaling SNs are coordinately expressed in disease-related tissues, which are tightly related to known pathological hallmarks of AD. Our findings suggest that genetic variation within glutamate signaling contributes to the remaining genetic risk of AD and support the notion that functional biological networks should be targeted in future therapies aimed to prevent or treat this devastating neurological disorder.