20 results on '"Aviles-Reyes A"'
Search Results
2. Amyloid Aggregation of Streptococcus mutans Cnm Influences Its Collagen-Binding Activity
- Author
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di Cologna, Nicholas M., primary, Samaddar, Sandip, additional, Valle, Carolina A., additional, Vargas, Jonathan, additional, Aviles-Reyes, Alejandro, additional, Morales, Joyce, additional, Ganguly, Tridib, additional, Pileggi, Roberta, additional, Brady, L. Jeannine, additional, Lemos, José A., additional, and Abranches, Jacqueline, additional
- Published
- 2021
- Full Text
- View/download PDF
3. Amyloid aggregation of Streptococcus mutans Cnm influences its collagen-binding activity
- Author
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Vargas, Valle, Samaddar, Abranches, Morales, Lemos, Aviles-Reyes, Ganguly, Pileggi, Brady, and de Mojana di Cologna
- Subjects
chemistry.chemical_classification ,Amyloid ,biology ,Biofilm ,Biofilm matrix ,biology.organism_classification ,Streptococcus mutans ,Congo red ,Bacterial adhesin ,chemistry.chemical_compound ,chemistry ,Biochemistry ,Glycoprotein ,Binding domain - Abstract
The glycosylated collagen- and laminin-binding surface adhesin Cnm is present in approximately 20% of S. mutans clinical isolates and is associated with systemic infections and increased caries risk. Other surface-associated collagen-binding proteins of S. mutans such as P1 and WapA have been demonstrated to form an amyloid quaternary structure with functional implications within biofilms. In silico analysis predicted that the β-sheet rich N-terminal collagen-binding domain (CBD) of Cnm has propensity for amyloid aggregation, whereas the threonine-rich C-terminal domain was predicted to be disorganized. In this study, thioflavin-T fluorescence and electron microscopy were used to show that Cnm forms amyloids either in its native glycosylated or recombinant non-glycosylated forms and that the CBD of Cnm is the main amyloidogenic unit of Cnm. We then performed a series of in vitro, ex vivo and in vivo assays to characterize the amylogenic properties of Cnm. In addition, Congo red birefringence indicated that Cnm is a major amyloidogenic protein of S. mutans biofilms. Competitive binding assays using collagen-coated microtiter plates and dental roots, a substrate rich in collagen, revealed that Cnm monomers inhibit S. mutans binding to collagenous substrates whereas Cnm amyloid aggregates lose this property. Thus, while Cnm contributes to recognition and initial binding of S. mutans to collagen-rich surfaces, Cnm amyloid aggregation appears to represent a mechanism to modulate this activity in mature biofilms.IMPORTANCEStreptococcus mutans is a keystone pathogen that promotes caries by acidifying the dental biofilm milieu. The collagen- and laminin-binding glycoprotein Cnm is a virulence factor found in about 20% of the clinical isolates of S. mutans. Expression of Cnm by S. mutans is associated with niche expansion, allowing colonization of multiple sites in the body including collagen-rich surfaces such as dentin and heart valves. Here, we demonstrate for the first time that Cnm function appears to be modulated by its aggregation status. As a monomer, its primary function is to promote attachment to collagenous substrates via its collagen binding domain (CBD). However, in later stages of biofilm maturation, the same CBD of Cnm self-assembles into amyloid fibrils, losing the ability to bind to collagen and likely becoming a component of the biofilm matrix. Our findings shed light into the role of functional amyloids in S. mutans pathobiology and ecology.
- Published
- 2021
4. Amyloid aggregation of Streptococcus mutans Cnm influences its collagen-binding activity
- Author
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de Mojana di Cologna, Nicholas, primary, Samaddar, Sandip, additional, Valle, Carolina A., additional, Vargas, Jonathan, additional, Aviles-Reyes, Alejandro, additional, Morales, Joyce, additional, Ganguly, Tridib, additional, Pileggi, Roberta, additional, Brady, L. Jeannine, additional, Lemos, José A., additional, and Abranches, Jacqueline, additional
- Published
- 2021
- Full Text
- View/download PDF
5. Intermittent hypoxia during sleep induces reactive gliosis and limited neuronal death in rats: implications for sleep apnea
- Author
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Aviles-Reyes, Rolando Xavier, Angelo, Maria Florencia, Villarreal, Alejandro, Rios, Hugo, Lazarowski, Alberto, and Ramos, Alberto Javier
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- 2010
- Full Text
- View/download PDF
6. Toma de decisiones y su relación con la satisfacción de la vida cotidiana en adolescentes y adultos jóvenes
- Author
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RUBEN AVILES REYES and MA DE LA CRUZ BERNARDA TELLEZ ALANIS
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4 [cti] ,61 [cti] - Abstract
Resumen La presente investigación tuvo como objetivo relacionar la toma de decisiones en adolescentes y adultos jóvenes con la satisfacción de las actividades de la vida cotidiana, a través de dos estudios. El primer estudio estuvo encaminado a la realización de dos instrumentos para la evaluación de la satisfacción de las actividades de la vida cotidiana en sus dimensiones, emocional, cognitiva y social, uno en adolescentes y otro en adultos jóvenes; se realizó un análisis factorial exploratorio y un análisis factorial confirmatorio a cada instrumento, los resultados indican que, las dimensiones emocional, cognitiva y social, si se ajustan con la satisfacción de las actividades de la vida cotidiana en cada una de las etapas del desarrollo humano estudiadas. El segundo estudio tuvo como finalidad evaluar y comparar la toma de decisiones y posteriormente relacionarla con la satisfacción de las actividades de la vida cotidiana entre los adolescentes y adultos jóvenes en las dimensiones emocional, cognitiva y social. Para la evaluación de la toma de decisiones, se realizó una prueba U de Mann-Whitney y para determinar la correlación, se realizaron dos análisis estadísticos de correlación de Spearman entre las variables. Los resultados indican diferencias significativas entre ambos grupos en la toma de decisiones, arriesgándose mas los adolescentes en el componente emocional y cognitivo, comparado con los adultos jóvenes, mientras que en el social los adolescentes consideran inadecuadas las acciones a pesar de que no exista una intención de causar daño, mientras que los adultos jóvenes, creen que es inadecuada la acción porque existe la intención clara de causar daño, a pesar de que los resultados o consecuencia hayan sido neutrales. Por último, las correlaciones encontradas significativamente, indican que los adolescentes al mostrarse satisfechos con las actividades de la vida cotidiana, mejoran su ejecución en las tareas que miden la toma de decisiones en su tres componentes: emocional, cognitivo y social, situación que no se pudo observar en los adultos jóvenes
- Published
- 2019
7. P1‐178: ASTROCYTIC OVEREXPRESSION OF NRF2 LEADS TO REDUCED DISEASE PROGRESSION IN APP/PS1 TRANSGENIC MICE
- Author
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Jeffrey S. Johnson, Rolando Xavier Aviles-Reyes, and Delinda Jonhson
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0301 basic medicine ,Genetically modified mouse ,Epidemiology ,business.industry ,Health Policy ,Disease progression ,03 medical and health sciences ,Psychiatry and Mental health ,Cellular and Molecular Neuroscience ,030104 developmental biology ,Developmental Neuroscience ,Cancer research ,Medicine ,Neurology (clinical) ,Geriatrics and Gerontology ,business - Published
- 2018
8. Detección de enfermedad renal aculta en habitantes del Barrio Fátima Rivas periodo Agosto 2018
- Author
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Aviles Reyes, Anielka Sofia, Gutiérrez Mena, Francisco Antonio, and Rodríguez Peña, Luis Carlos
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WJ 140-160 Enfermedades Urológicas ,WG 200-460 Corazón. Enfermedades del corazón - Abstract
La enfermedad renal oculta (ERO) define los estadios más iniciales de insuficiencia renal, para establecer el diagnostico se utilizan métodos no convencionales que pueden ser aplicados en atención primaria para la detección temprana. Material y método: Estudio descriptivo, transversal retrospectivo. La muestra fue de 300 personas, se aplicó una encuesta estructurada, se les tomó la presión arterial, pesó y talla, se obtuvo una muestra de sangre y orina, se rotularon y almacenaron para su traslado al laboratorio clínico de la Facultad de Medicina donde se procesaron y realizaron análisis general de orina, creatininuria y proteinuria en orina casual, creatinina sérica y nitrógeno de urea. Se estimó la tasa de filtración glomerular mediante la fórmula de CKD-EPI y el cociente proteína-creatinina. Resultados: La edad media fue de 33,34 años, predominó el sexo femenino. Con la fórmula de CKD-EPI se detectó una disminución leve del filtrado en un 27%, disminución moderada en el 33% y no hubo disminución severa. Se estimó que de este grupo la ERO representa el 33%. Un 30% de los pacientes con ERO son hipertensos y un 3% tiene diabetes tipo 2 e hipertensión. Conclusiones: La enfermedad renal oculta se detectó en el 33% de los participantes, todos se encontraban en estadio III de enfermedad renal, predominó en personas mayores de 30 años y en mujeres. Se recomienda la utilización de fórmulas para determinar el FG, sobre todo en mujeres y en cualquier edad, ya que las alteraciones renales se pueden manifestar incluso antes de llegar a una edad muy avanzada
- Published
- 2018
9. P1‐178: ASTROCYTIC OVEREXPRESSION OF NRF2 LEADS TO REDUCED DISEASE PROGRESSION IN APP/PS1 TRANSGENIC MICE
- Author
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Aviles-Reyes, Rolando Xavier, primary, Jonhson, Delinda, additional, and Johnson, Jeffrey, additional
- Published
- 2018
- Full Text
- View/download PDF
10. S100B alters neuronal survival and dendrite extension via RAGE-mediated NF-κB signaling
- Author
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Rolando Xavier Aviles Reyes, Alberto Javier Ramos, Maria Florencia Angelo, Analía Reinés, and Alejandro Villarreal
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Penumbra ,Glutamate receptor ,Biology ,medicine.disease ,Biochemistry ,RAGE (receptor) ,Brain ischemia ,Cellular and Molecular Neuroscience ,medicine.anatomical_structure ,Cerebral cortex ,medicine ,Dendrite extension ,Signal transduction ,Receptor ,Neuroscience - Abstract
S100B is a soluble protein secreted by astrocytes that exerts pro-survival or pro-apoptotic effects depending on the concentration reached in the extracellular millieu. The S100B receptor termed RAGE (for receptor for advanced end glycation products) is highly expressed in the developing brain but is undetectable in normal adult brain. In this study, we show that RAGE expression is induced in cortical neurons of the ischemic penumbra. Increased RAGE expression was also observed in primary cortical neurons exposed to excitotoxic glutamate (EG). S100B exerts effects on survival pathways and neurite extension when the cortical neurons have been previously exposed to EG and these S100B effects were prevented by anti-RAGE blocking antibodies. Furthermore, nuclear factor kappa B (NF-κB) is activated by S100B in a dose- and RAGE-dependent manner and neuronal death induced by NF-κB inhibition was prevented by S100B that restored NF-κB activation levels. Together, these findings suggest that excitotoxic damage can induce RAGE expression in neurons from ischemic penumbra and demonstrate that cortical neurons respond to S100B through engagement of RAGE followed by activation of NF-κB signaling. In addition, basal NF-κB activity in neurons is crucial to modulate the extent of pro-survival or pro-death S100B effects.
- Published
- 2011
11. p75NTRExpression is induced in isolated neurons of the penumbra after ischemia by cortical devascularization
- Author
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Alberto Javier Ramos, Maria Florencia Angelo, Rolando Xavier Aviles-Reyes, Analía Reinés, Alejandro Villarreal, and Phil Barker
- Subjects
musculoskeletal diseases ,Brain Infarction ,Male ,Sp1 Transcription Factor ,Neurotoxins ,Central nervous system ,Ischemia ,Apoptosis ,Nerve Tissue Proteins ,Receptors, Nerve Growth Factor ,Brain Ischemia ,Cellular and Molecular Neuroscience ,Stress, Physiological ,medicine ,Animals ,Low-affinity nerve growth factor receptor ,Receptors, Growth Factor ,Rats, Wistar ,skin and connective tissue diseases ,Cells, Cultured ,Cerebral Cortex ,Neurons ,Sp1 transcription factor ,biology ,Caspase 3 ,Penumbra ,Glutamate receptor ,Cerebral Arteries ,medicine.disease ,biological factors ,Rats ,Up-Regulation ,Adaptor Proteins, Vesicular Transport ,Cerebrovascular Disorders ,Disease Models, Animal ,medicine.anatomical_structure ,nervous system ,Nerve Degeneration ,biology.protein ,sense organs ,Neuroscience ,Neurotrophin - Abstract
The p75 neurotrophin receptor (p75(NTR)) is involved in neuronal functions ranging from induction of apoptosis and growth inhibition to the promotion of survival. p75(NTR) expression is induced in the central nervous system (CNS) by a range of pathological conditions, where it seems to have a role in neuronal death and axonal growth inhibition. The cellular mechanisms driving p75(NTR) expression in cell lines and primary neurons is Sp1 dependent (Ramos et al. [2007] J. Neurosci. 27:1498). In this study, we analyzed the spatiotemporal profile of p75(NTR) expression after an ischemic lesion induced by cortical devascularization (CD). Our results show that p75(NTR) expression occurs in isolated neurons of the ischemic lesion site. The p75(NTR+) neurons presented morphological alterations and active caspase-3 staining. Some p75(NTR+) neurons were also positive for sortilin. The peak of p75(NTR) expression was localized 3 days postlesion (3DPL) in the penumbra. Sp1 transcription factor nuclear localization was observed in p75(NTR+) neurons. The overall level of Sp1 expression was increased until 14DPL on the ipsilateral hemisphere. With primary cortical neurons, we demonstrated that p75(NTR) expression is induced by excitotoxic stress and correlated with increased Sp1 abundance. We conclude that p75(NTR) expression is localized in selected neurons of the ischemic lesion and that these neurons are probably condemned to apoptotic cell death. In primary neuronal culture, it is clear that excitotoxity and Sp1 are involved in induction of p75(NTR) expression, although, in vivo, some additional mechanisms are likely to be involved in the control of p75(NTR) expression in specific neurons in Vivo. (C) 2009 Wiley-Liss, Inc.
- Published
- 2009
12. Pro-inflammatory Analysis of Macrophages in Contact with Titanium Particles and Porphyromonas gingivalis
- Author
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Dodo, Cindy Goes, primary, Meirelles, Luiz, additional, Aviles-Reyes, Alejandro, additional, Ruiz, Karina Gonzalez Silvério, additional, Abranches, Jacqueline, additional, and Cury, Altair Antoninha Del Bel, additional
- Published
- 2017
- Full Text
- View/download PDF
13. The proinflammatory RAGE/NF-κB pathway is involved in neuronal damage and reactive gliosis in a model of sleep apnea by intermittent hypoxia
- Author
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Alberto Javier Ramos, Silvia Alvarez, Virginia Vanasco, Alejandra Inés Aguirre, Alejandro Villarreal, Diana Jerusalinsky, Philip A. Barker, Rolando Xavier Aviles Reyes, Maria Florencia Angelo, Matias Eliseo Melendez, Alberto L. Epstein, Jeronimo Lukin, Facultad de Medicina [Buenos Aires], Universidad de Buenos Aires [Buenos Aires] (UBA), Virus enveloppés, vecteurs et immunothérapie – Enveloped viruses, Vectors and Immuno-therapy (EVIR), Centre International de Recherche en Infectiologie (CIRI), École normale supérieure de Lyon (ENS de Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure de Lyon (ENS de Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centro de Estudios Farmacológicos y Botánicos [Buenos Aires] (CEFYBO), Consejo Nacional de Investigaciones Científicas y Técnicas [Buenos Aires] (CONICET)-Facultad de Medicina [Buenos Aires], Universidad de Buenos Aires [Buenos Aires] (UBA)-Universidad de Buenos Aires [Buenos Aires] (UBA), Montreal Neurological Institute and Hospital, McGill University = Université McGill [Montréal, Canada], Centre International de Recherche en Infectiologie - UMR (CIRI), Institut National de la Santé et de la Recherche Médicale (INSERM)-École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS), École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), and Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)
- Subjects
Male ,Receptor for Advanced Glycation End Products ,Wistar ,Hippocampus ,lcsh:Medicine ,Biochemistry ,RAGE (receptor) ,chemistry.chemical_compound ,Immunologic ,Receptors ,Gliosis ,Receptors, Immunologic ,Receptor ,lcsh:Science ,Hypoxia ,RAGE/NF-κB PATHWAY ,Neurons ,Multidisciplinary ,NF-kappa B ,Intermittent hypoxia ,Neurochemistry ,3. Good health ,Otras Ciencias Médicas ,medicine.anatomical_structure ,[SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology ,[SDV.IMM]Life Sciences [q-bio]/Immunology ,purl.org/becyt/ford/3 [https] ,Research Article ,CIENCIAS MÉDICAS Y DE LA SALUD ,Neurite ,Central nervous system ,purl.org/becyt/ford/3.5 [https] ,Proinflammatory cytokine ,Sleep Apnea Syndromes ,medicine ,Animals ,Rats, Wistar ,Animal ,lcsh:R ,Biology and Life Sciences ,NF-κB ,[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology ,Rats ,Disease Models, Animal ,chemistry ,REACTIVE GLIOSIS ,Immunology ,Disease Models ,Cancer research ,NEURONAL DAMAGE ,lcsh:Q ,Molecular Neuroscience ,Neuroscience - Abstract
Sleep apnea (SA) causes long-lasting changes in neuronal circuitry, which persist even in patients successfully treated for the acute effects of the disease. Evidence obtained from the intermittent hypoxia (IH) experimental model of SA has shown neuronal death, impairment in learning and memory and reactive gliosis that may account for cognitive and structural alterations observed in human patients. However, little is known about the mechanism controlling these deleterious effects that may be useful as therapeutic targets in SA. The Receptor for Advanced Glycation End products (RAGE) and its downstream effector Nuclear Factor Kappa B (NF-κB) have been related to neuronal death and astroglial conversion to the pro-inflammatory neurodegenerative phenotype. RAGE expression and its ligand S100B were shown to be increased in experimental models of SA. We here used dissociated mixed hippocampal cell cultures and male Wistar rats exposed to IH cycles and observed that NF-κB is activated in glial cells and neurons after IH. To disclose the relative contribution of the S100B/RAGE/NF-κB pathway to neuronal damage and reactive gliosis after IH we performed sequential loss of function studies using RAGE or S100B neutralizing antibodies, a herpes simplex virus (HSV)-derived amplicon vector that induces the expression of RAGEΔcyto (dominant negative RAGE) and a chemical blocker of NF-κB. Our results show that NF-κB activation peaks 3 days after IH exposure, and that RAGE or NF-κB blockage during this critical period significantly improves neuronal survival and reduces reactive gliosis. Both in vitro and in vivo, S100B blockage altered reactive gliosis but did not have significant effects on neuronal survival. We conclude that both RAGE and downstream NF-κB signaling are centrally involved in the neuronal alterations found in SA models, and that blockage of these pathways is a tempting strategy for preventing neuronal degeneration and reactive gliosis in SA. Fil: Angelo, María Florencia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia ; Argentina Fil: Aguirre, Alejandra Inés. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia ; Argentina Fil: Aviles Reyes, Rolando Xavier. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia ; Argentina Fil: Villarreal, Alejandro. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia ; Argentina Fil: Lukin, Jeronimo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia ; Argentina Fil: Melendez, Matías. Inserm; Francia. Centre National de la Recherche Scientifique; Francia. Université Claude Bernard Lyon 1; Francia Fil: Vanasco, Virginia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Bioquímica y Medicina Molecular; Argentina Fil: Barker, Philip A.. McGill University; Canadá Fil: Alvarez, Silvia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Bioquímica y Medicina Molecular; Argentina Fil: Epstein, Alberto Luis. Inserm; Francia. Centre National de la Recherche Scientifique; Francia. Université Claude Bernard Lyon 1; Francia Fil: Jerusalinsky, Diana Alicia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia ; Argentina Fil: Ramos, Alberto Javier. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia ; Argentina
- Published
- 2014
14. Simultaneous spatiotemporal mapping of in situ pH and bacterial activity within an intact 3D microcolony structure
- Author
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Hwang, Geelsu, primary, Liu, Yuan, additional, Kim, Dongyeop, additional, Sun, Victor, additional, Aviles-Reyes, Alejandro, additional, Kajfasz, Jessica K., additional, Lemos, Jose A., additional, and Koo, Hyun, additional
- Published
- 2016
- Full Text
- View/download PDF
15. ASTROCYTIC OVEREXPRESSION OF NRF2 LEADS TO REDUCED DISEASE PROGRESSION IN APP/PS1 TRANSGENIC MICE
- Author
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Aviles-Reyes, Rolando Xavier, Jonhson, Delinda, and Johnson, Jeffrey
- Published
- 2018
- Full Text
- View/download PDF
16. S100B alters neuronal survival and dendrite extension via RAGE-mediated NF-κB signaling
- Author
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Alejandro, Villarreal, Rolando X, Aviles Reyes, Maria Florencia, Angelo, Analia G, Reines, and Alberto Javier, Ramos
- Subjects
Cerebral Cortex ,Male ,Neurons ,Time Factors ,Cell Survival ,Receptor for Advanced Glycation End Products ,S100 Proteins ,NF-kappa B ,Glutamic Acid ,Sulfadiazine ,Dendrites ,Embryo, Mammalian ,Antibodies ,Brain Ischemia ,Rats ,Gene Expression Regulation ,Phosphopyruvate Hydratase ,Animals ,Drug Interactions ,Enzyme Inhibitors ,Rats, Wistar ,Receptors, Immunologic ,Cells, Cultured ,Signal Transduction - Abstract
S100B is a soluble protein secreted by astrocytes that exerts pro-survival or pro-apoptotic effects depending on the concentration reached in the extracellular millieu. The S100B receptor termed RAGE (for receptor for advanced end glycation products) is highly expressed in the developing brain but is undetectable in normal adult brain. In this study, we show that RAGE expression is induced in cortical neurons of the ischemic penumbra. Increased RAGE expression was also observed in primary cortical neurons exposed to excitotoxic glutamate (EG). S100B exerts effects on survival pathways and neurite extension when the cortical neurons have been previously exposed to EG and these S100B effects were prevented by anti-RAGE blocking antibodies. Furthermore, nuclear factor kappa B (NF-κB) is activated by S100B in a dose- and RAGE-dependent manner and neuronal death induced by NF-κB inhibition was prevented by S100B that restored NF-κB activation levels. Together, these findings suggest that excitotoxic damage can induce RAGE expression in neurons from ischemic penumbra and demonstrate that cortical neurons respond to S100B through engagement of RAGE followed by activation of NF-κB signaling. In addition, basal NF-κB activity in neurons is crucial to modulate the extent of pro-survival or pro-death S100B effects.
- Published
- 2011
17. Intermittent Hypoxia During Sleep Induces Reactive Gliosis And Limited Neuronal Death In Rats: Implications For Sleep Apnea
- Author
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Hugo Rios, Maria Florencia Angelo, Alberto Lazarowski, Alejandro Villarreal, Rolando Xavier Aviles-Reyes, and Alberto Javier Ramos
- Subjects
Male ,Programmed cell death ,medicine.medical_specialty ,Time Factors ,Central nervous system ,Nerve Tissue Proteins ,Hippocampal formation ,Biochemistry ,Cellular and Molecular Neuroscience ,Sleep Apnea Syndromes ,Internal medicine ,Proliferating Cell Nuclear Antigen ,medicine ,Animals ,Gliosis ,Rats, Wistar ,Neurons ,Cell Death ,business.industry ,Brain ,Intermittent hypoxia ,Hypoxia (medical) ,Rats ,Disease Models, Animal ,medicine.anatomical_structure ,Endocrinology ,nervous system ,Cerebral cortex ,Caspases ,Neuroglia ,medicine.symptom ,business ,Neuroscience - Abstract
Sleep apnea (SA) can be effectively managed in humans but it is recognized that when left untreated, SA causes long-lasting changes in neuronal circuitry in the brain. Recent neuroimaging studies gave suggested that these neuronal changes are also present even in patients successfully treated for the acute effects of SA. The cellular mechanisms that account for these changes are not certain but animal models of intermittent hypoxia (IH) during sleep have shown neuronal death and impairment in learning and memory. Reactive gliosis has a drastic effect on neuronal survival and circuitry and in this study we examined the neuro-glial response in brain areas affected by SA. Glial and neuronal alterations were analyzed after 1, 3, 5 and 10 days of exposure to IH (8 h/day during the sleep phase, cycles of 6 min each, 10-21% O-2) and observed significant astroglial hyperplasia and hypertrophy in parietal brain cortex and hippocampus by studying gliofibrillary acidic protein, Vimentin, S100B and proliferating cell nuclear antigen expression. In addition, altered morphology, reduced dendrite branching and caspase activation were observed in the CA-1 hippocampal and cortical ( layers IV-V) pyramidal neurons at short exposure times (1-3 days). Surprisingly, longer exposure to IH reduced the neuronal death rate and increased neuronal branching in the presence of persistent reactive gliosis. Up-regulation of hypoxia inducible factor 1 alpha (HIF-1 alpha) and mdr-1, a HIF-1 alpha target gene, were observed and increased expression of receptor for advanced end glycated products and its binding partner S100B were also noted. Our results show that a low number of hypoxic cycles induce reactive gliosis and neuronal death whereas continuous exposure to IH cycles reduced the rate of neuronal death and induced neuronal branching on surviving neurons. We hypothesize that HIF-1 alpha and S100B glial factor may improve neuronal survival under hypoxic conditions and propose that the death/survival/re-growth process observed here may underlie brain circuitry changes in humans with SA.
- Published
- 2010
18. The role of clinical variables, neuropsychological performance and SLC6A4 and COMT gene polymorphisms on the prediction of early response to fluoxetine in major depressive disorder
- Author
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Gudayol-Ferré, Esteve, Herrera-Guzmán, Ixchel, Camarena, Beatriz, Cortés-Penagos, Carlos, Herrera-Abarca, Jorge E., Martínez-Medina, Patricia, Cruz, David, Hernández, Sandra, Genis, Alma, Carrillo-Guerrero, Mariana Y., Avilés Reyes, Rubén, and Guàrdia-Olmos, Joan
- Published
- 2010
- Full Text
- View/download PDF
19. S100B alters neuronal survival and dendrite extension via RAGE-mediated NF-κB signaling
- Author
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Villarreal, Alejandro, primary, Aviles Reyes, Rolando X., additional, Angelo, Maria Florencia, additional, Reines, Analia G., additional, and Ramos, Alberto Javier, additional
- Published
- 2011
- Full Text
- View/download PDF
20. p75NTRExpression is induced in isolated neurons of the penumbra after ischemia by cortical devascularization
- Author
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Angelo, Maria Florencia, primary, Aviles-Reyes, Rolando X., additional, Villarreal, Alejandro, additional, Barker, Phil, additional, Reines, Analia G., additional, and Ramos, Alberto Javier, additional
- Published
- 2009
- Full Text
- View/download PDF
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