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13 results on '"Golbano, Arantxa"'

5. Neuron type‐specific increase in lamin B1 contributes to nuclear dysfunction in Huntington’s disease

Author

Alcalá‐Vida, Rafael, primary, Garcia‐Forn, Marta, additional, Castany‐Pladevall, Carla, additional, Creus‐Muncunill, Jordi, additional, Ito, Yoko, additional, Blanco, Enrique, additional, Golbano, Arantxa, additional, Crespí‐Vázquez, Kilian, additional, Parry, Aled, additional, Slater, Guy, additional, Samarajiwa, Shamith, additional, Peiró, Sandra, additional, Di Croce, Luciano, additional, Narita, Masashi, additional, and Pérez‐Navarro, Esther, additional

Published
2020
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6. Imidazoline ligand BU224 reverses cognitive deficits, reduces microgliosis and enhances synaptic connectivity in a mouse model of Alzheimer's disease

Author

Mirzaei, Nazanin, primary, Mota, Bibiana C., additional, Birch, Amy M., additional, Davis, Nicola, additional, Romero‐Molina, Carmen, additional, Katsouri, Loukia, additional, Palmer, Emily O.C., additional, Golbano, Arantxa, additional, Riggall, Laura J., additional, Nagy, Istvan, additional, Tyacke, Robin, additional, Nutt, David J., additional, and Sastre, Magdalena, additional

Published
2020
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7. Imidazoline ligand BU224 reverses cognitive deficits, reduces microgliosis and enhances synaptic connectivity in a mouse model of Alzheimer's disease.

Author

Mirzaei, Nazanin, Mota, Bibiana C., Birch, Amy M., Davis, Nicola, Romero‐Molina, Carmen, Katsouri, Loukia, Palmer, Emily O.C., Golbano, Arantxa, Riggall, Laura J., Nagy, Istvan, Tyacke, Robin, Nutt, David J., Sastre, Magdalena, and Romero-Molina, Carmen

Subjects
ALZHEIMER'S disease, IMIDAZOLINES, AMYLOID beta-protein precursor, ANIMAL disease models, TRANSGENIC mice, DENDRITIC spines, BIOLOGICAL models, RESEARCH, ANIMAL experimentation, RESEARCH methodology, PROTEIN precursors, COGNITION, MEDICAL cooperation, EVALUATION research, IMIDAZOLES, COMPARATIVE studies, RESEARCH funding, MICE, LIGANDS (Biochemistry), PEPTIDES
Abstract

Background and Purpose: Activation of type 2 imidazoline receptors has been shown to exhibit neuroprotective properties including anti-apoptotic and anti-inflammatory effects, suggesting a potential therapeutic value in Alzheimer's disease (AD). Here, we explored the effects of the imidazoline-2 ligand BU224 in a model of amyloidosis.Experimental Approach: Six-month-old female transgenic 5XFAD and wild-type (WT) mice were treated intraperitoneally with 5-mg·kg-1 BU224 or vehicle twice a day for 10 days. Behavioural tests were performed for cognitive functions and neuropathological changes were investigated by immunohistochemistry, Western blot, elisa and qPCR. Effects of BU224 on amyloid precursor protein (APP) processing, spine density and calcium imaging were analysed in brain organotypic cultures and N2a cells.Key Results: BU224 treatment attenuated spatial and perirhinal cortex-dependent recognition memory deficits in 5XFAD mice. Fear-conditioning testing revealed that BU224 also improved both associative learning and hippocampal- and amygdala-dependent memory in transgenic but not in WT mice. In the brain, BU224 reduced levels of the microglial marker Iba1 and pro-inflammatory cytokines IL-1β and TNF-α and increased the expression of astrocytic marker GFAP in 5XFAD mice. These beneficial effects were not associated with changes in amyloid pathology, neuronal apoptosis, mitochondrial density, oxidative stress or autophagy markers. Interestingly, ex vivo and in vitro studies suggested that BU224 treatment increased the size of dendritic spines and induced a threefold reduction in amyloid-β (Aβ)-induced functional changes in NMDA receptors.Conclusion and Implications: Sub-chronic treatment with BU224 restores memory and reduces inflammation in transgenic AD mice, at stages when animals display severe pathology. [ABSTRACT FROM AUTHOR]

Published
2021
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9. CREB regulates distinct adaptive transcriptional programs in astrocytes and neurons

Author

Generalitat de Catalunya, European Commission, Ministerio de Economía y Competitividad (España), Fundación Alicia Koplowitz, Instituto de Salud Carlos III, Ministerio de Ciencia e Innovación (España), Generalitat Valenciana, Brain and Behavior Research Foundation, Pardo, Luis A., Valor, Luis Miguel, Eraso-Pichot, Abel, Barco, Ángel, Golbano, Arantxa, Hardingham, Giles E., Masgrau, Roser, Galea, Elena, Generalitat de Catalunya, European Commission, Ministerio de Economía y Competitividad (España), Fundación Alicia Koplowitz, Instituto de Salud Carlos III, Ministerio de Ciencia e Innovación (España), Generalitat Valenciana, Brain and Behavior Research Foundation, Pardo, Luis A., Valor, Luis Miguel, Eraso-Pichot, Abel, Barco, Ángel, Golbano, Arantxa, Hardingham, Giles E., Masgrau, Roser, and Galea, Elena

Abstract

The cyclic AMP response element binding protein (CREB) is a primary hub of activity-driven genetic programs in neurons controlling plasticity, neurogenesis and survival. By contrast, the gene networks coordinated by CREB in astrocytes are unknown despite the fact that the astrocytic CREB is also activity-driven and neuroprotective. Herein we identified the transcriptional programs regulated by CREB in astrocytes as compared to neurons using, as study materials, transcriptome databases of astrocyte exposed to well-known activators of CREB-dependent transcription as well as publicly available transcriptomes of neuronal cultures. Functional CREB signatures were extracted from the transcriptomes using Gene Ontology, adult-brain gene lists generated by Translating Ribosome Affinity Purification (TRAP) and CREB-target gene repositories. We found minimal overlap between CREB signatures in astrocytes and neurons. In astrocytes, the top triad of functions regulated by CREB consists of ‘Gene expression’, ‘Mitochondria’, and ‘Signalling’, while in neurons it is ‘Neurotransmission’, ‘Signalling’ and ‘Gene expression’, the latter two being represented by different genes from those in astrocytes. The newly generated databases will provide a tool to explore novel means whereby CREB impinges on brain functions requiring adaptive, long-lasting changes by coordinating transcriptional cascades in astrocytes.

Published
2017

10. Targeted activation of CREB in reactive astrocytes is neuroprotective in focal acute cortical injury

Author

Pardo, Luis A., Schlüter, Agatha, Valor, Luis Miguel, Barco, Ángel, Giralt, Mercedes, Golbano, Arantxa, Hidalgo, Juan, Jia, Peilin, Zhao, Zhongming, Jové, Mariona, Portero-Otin, Manuel, Ruiz, Montserrat, Giménez-Llort, Lydia, Masgrau, Roser, Pujol, Aurora, and Galea, Elena

Abstract

The clinical challenge in acute injury as in traumatic brain injury (TBI) is to halt the delayed neuronal loss that occurs hours and days after the insult. Here we report that the activation of CREB-dependent transcription in reactive astrocytes prevents secondary injury in cerebral cortex after experimental TBI. The study was performed in a novel bitransgenic mouse in which a constitutively active CREB, VP16-CREB, was targeted to astrocytes with the Tet-Off system. Using histochemistry, qPCR, and gene profiling we found less neuronal death and damage, reduced macrophage infiltration, preserved mitochondria, and rescued expression of genes related to mitochondrial metabolism in bitransgenic mice as compared to wild type littermates. Finally, with meta-analyses using publicly available databases we identified a core set of VP16-CREB candidate target genes that may account for the neuroprotective effect. Enhancing CREB activity in astrocytes thus emerges as a novel avenue in acute brain post-injury therapeutics.

Published
2016

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