43 results on '"Gomez-Pinedo U"'
Search Results
2. Exonic variants of the P2RX7 gene in familial multiple sclerosis
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Gómez-Pinedo, U., Torre-Fuentes, L., Matías-Guiu, J.A., Pytel, V., Ojeda-Hernández, D.D., Selma-Calvo, B., Montero-Escribano, P., Vidorreta-Ballesteros, L., and Matías-Guiu, J.
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- 2022
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3. Variant rs4149584 (R92Q) of the TNFRSF1A gene in patients with familial multiple sclerosis
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Gomez-Pinedo, U., Matías-Guiu, J.A., Torre-Fuentes, L., Montero-Escribano, P., Hernández-Lorenzo, L., Pytel, V., Maietta, P., Alvarez, S., Sanclemente-Alamán, I., Moreno-Jimenez, L., Ojeda-Hernandez, D., Villar-Gómez, N., Benito-Martin, M.S., Selma-Calvo, B., Vidorreta-Ballesteros, L., Madrid, R., and Matías-Guiu, J.
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- 2022
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4. NG2 and GFAP co-expression after differentiation in cells transfected with mutant GFAP and in undifferentiated glioma cells
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Gómez-Pinedo, U., Sirerol-Piquer, S., Durán-Moreno, M., Matias-Guiu, J.A., Barcia, J.A., García-Verdugo, J.M., and Matias-Guiu, J.
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- 2020
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5. Should we expect neurological symptoms in the SARS-CoV-2 epidemic?
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Matías-Guiu, J., Gomez-Pinedo, U., Montero-Escribano, P., Gomez-Iglesias, P., Porta-Etessam, J., and Matias-Guiu, J.A.
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- 2020
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6. Human recombinant erythropoietin reduces sensorimotor dysfunction and cognitive impairment in rat models of chronic kidney disease
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Reza-Zaldívar, E.E., Sandoval-Avila, S., Gutiérrez-Mercado, Y.K., Vázquez-Méndez, E., Canales-Aguirre, A.A., Esquivel-Solís, H., Gómez-Pinedo, U., and Márquez-Aguirre, A.L.
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- 2020
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7. Experimental models of demyelination and remyelination
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Torre-Fuentes, L., Moreno-Jiménez, L., Pytel, V., Matías-Guiu, J.A., Gómez-Pinedo, U., and Matías-Guiu, J.
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- 2020
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8. Neuroprotective effects of phytochemicals on dopaminergic neuron cultures
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Sandoval-Avila, S., Diaz, N.F., Gómez-Pinedo, U., Canales-Aguirre, A.A., Gutiérrez-Mercado, Y.K., Padilla-Camberos, E., Marquez-Aguirre, A.L., and Díaz-Martínez, N.E.
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- 2019
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9. Myelin changes in Alexander disease
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Gómez-Pinedo, U., Duran-Moreno, M., Sirerol-Piquer, S., and Matias-Guiu, J.
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- 2018
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10. Histological changes in the rat brain and spinal cord following prolonged intracerebroventricular infusion of cerebrospinal fluid from amyotrophic lateral sclerosis patients are similar to those caused by the disease
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Gómez-Pinedo, U., Galán, L., Yañez, M., Matias-Guiu, J., Valencia, C., Guerrero-Sola, A., Lopez-Sosa, F., Brin, J.R., Benito-Martin, M.S., Leon-Espinosa, G., Vela-Souto, A., Lendinez, C., Guillamón-Vivancos, T., Matias-Guiu, J.A., Arranz-Tagarro, J.A., Barcia, J.A., and Garcia, A.G.
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- 2018
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11. Vitamin D and remyelination in multiple sclerosis
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Matías-Guíu, J., Oreja-Guevara, C., Matias-Guiu, J.A., and Gomez-Pinedo, U.
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- 2018
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12. Astrocytes in neurodegenerative diseases (I): function and molecular description
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Guillamón-Vivancos, T., Gómez-Pinedo, U., and Matías-Guiu, J.
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- 2015
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13. Cellular changes in motor neuron cell culture produced by cytotoxic cerebrospinal fluid from patients with amyotrophic lateral sclerosis
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Gomez-Pinedo, U., Yáñez, M., Matías-Guiu, J., Galán, L., Guerrero-Sola, A., Benito-Martin, M.S., Vela, Á., Arranz-Tagarro, J.A., and García, A.G.
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- 2014
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14. Molecular aspects of hepatic encephalopathy
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Márquez-Aguirre, A.L., Canales-Aguirre, A.A., Gómez-Pinedo, U., and Gálvez-Gastélum, F.J.
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- 2010
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15. Proinflammatory cytokines and apoptosis following glutamate-induced excitotoxicity mediated by p38 MAPK in the hippocampus of neonatal rats
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Chaparro-Huerta, V., Rivera-Cervantes, M.C., Flores-Soto, M.E., Gómez-Pinedo, U., and Beas-Zárate, C.
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- 2005
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16. Biomaterial- and stem cell–based treatment strategies for diseases of the central nervous system
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Canales-Aguirre, A., Mateos-Díaz, J.C., Matias-Guiu, J., and Gomez-Pinedo, U.
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- 2022
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17. Cell therapy in amyotrophic lateral sclerosis: science and controversy
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Galán, L., Guerrero-Sola, A., Gómez-Pinedo, U., and Matias-Guiu, J.
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- 2010
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18. Histological and ultrastructural comparison of cauterization and thrombosis stroke models in immune-deficient mice
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Mora-Lee Silvia, Sirerol-Piquer Ma Salomé, Gutiérrez-Pérez María, López Tania, Casado-Nieto Mayte, Jauquicoam Carlos, Abizanda Gloria, Romaguera-Ros Miriam, Gomez-Pinedo Ulises, Prósper Felipe, and García-Verdugo José-Manuel
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cerebral ischemia ,scar ,thrombosis ,cauterization ,SVZ, gliosis, inflammation ,Therapeutics. Pharmacology ,RM1-950 - Abstract
Abstract Background Stroke models are essential tools in experimental stroke. Although several models of stroke have been developed in a variety of animals, with the development of transgenic mice there is the need to develop a reliable and reproducible stroke model in mice, which mimics as close as possible human stroke. Methods BALB/Ca-RAG2-/-γc-/- mice were subjected to cauterization or thrombosis stroke model and sacrificed at different time points (48hr, 1wk, 2wk and 4wk) after stroke. Mice received BrdU to estimate activation of cell proliferation in the SVZ. Brains were processed for immunohistochemical and EM. Results In both stroke models, after inflammation the same glial scar formation process and damage evolution takes place. After stroke, necrotic tissue is progressively removed, and healthy tissue is preserved from injury through the glial scar formation. Cauterization stroke model produced unspecific damage, was less efficient and the infarct was less homogeneous compared to thrombosis infarct. Finally, thrombosis stroke model produces activation of SVZ proliferation. Conclusions Our results provide an exhaustive analysis of the histopathological changes (inflammation, necrosis, tissue remodeling, scarring...) that occur after stroke in the ischemic boundary zone, which are of key importance for the final stroke outcome. This analysis would allow evaluating how different therapies would affect wound and regeneration. Moreover, this stroke model in RAG 2-/- γC -/- allows cell transplant from different species, even human, to be analyzed.
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- 2011
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19. Beneficial effects of α-lipoic acid plus vitamin E on neurological deficit, reactive gliosis and neuronal remodeling in the penumbra of the ischemic rat brain
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Gonzalez-Perez, O., Gonzalez-Castañeda, R.E., Huerta, M., Luquin, S., Gomez-Pinedo, U., Sanchez-Almaraz, E., Navarro-Ruiz, A., and Garcia-Estrada, J.
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CEREBRAL ischemia , *LIPOIC acid , *EMBOLISMS - Abstract
During cerebral ischemia-reperfusion, the enhanced production of oxygen-derived free radicals contributes to neuronal death. The antioxidants α-lipoic acid and vitamin E have shown synergistic effects against lipid peroxidation by oxidant radicals in several pathological conditions. A thromboembolic stroke model in rats was used to analyze the effects of this mixture under two oral treatments: intensive and prophylactic. Neurological functions, glial reactivity and neuronal remodeling were assessed after experimental infarction. Neurological recovery was only found in the prophylactic group, and both antioxidant schemes produced down-regulation of astrocytic and microglial reactivity, as well as higher neuronal remodeling in the penumbra area, as compared with controls. The beneficial effects of this antioxidant mixture suggest that it may be valuable for the treatment of cerebral ischemia in humans. [Copyright &y& Elsevier]
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- 2002
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20. Thermosensitive chitosan-based hydrogel: A vehicle for overcoming the limitations of nose-to-brain cell therapy.
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Ojeda-Hernández DD, Velasco-Lozano S, Fraile JM, Mateos-Díaz JC, Rojo FJ, Benito-Martín MS, Selma-Calvo B, Fuente-Martín S, García-Martín M, Larriba-González MT, Hernández-Sapiéns MA, Canales-Aguirre AA, Matias-Guiu JA, Matias-Guiu J, and Gomez-Pinedo U
- Abstract
Cell therapy is a promising strategy for treating neurological pathologies but requires invasive methods to bypass the blood-brain barrier restrictions. The nose-to-brain route has been presented as a direct and less invasive alternative to access the brain. The primary limitations of this route are low retention in the olfactory epithelium and poor cell survival in the harsh conditions of the nasal cavity. Thus, using chitosan-based hydrogel as a vehicle is proposed in this work to overcome the limitations of nose-to-brain cell administration. The hydrogel's design was driven to achieve gelification in response to body temperature and a mucosa-interacting chemical structure biocompatible with cells. The hydrogel showed a < 30 min gelation time at 37 °C and >95 % biocompatibility with 2D and 3D cultures of mesenchymal stromal cells. Additionally, the viability, stability, and migration capacity of oligodendrocyte precursor cells (OPCs) within the hydrogel were maintained in vitro for up to 72 h. After the intranasal administration of the OPCs-containing hydrogel, histological analysis showed the presence of viable cells in the nasal cavity for up to 72 h post-administration in healthy athymic mice. These results demonstrate the hydrogel's capacity to increase the residence time in the nasal cavity while providing the cells with a favorable environment for their viability. This study presents for the first time the use of thermosensitive hydrogels in nose-to-brain cell therapy, opening the possibility of increasing the delivery efficiency in future approaches in translational medicine. STATEMENT OF SIGNIFICANCE: This work highlights the potential of biomaterials, specifically hydrogels, in improving the effectiveness of cell therapy administered through the nose. The nose-to-brain route has been suggested as a non-invasive way to directly access the brain. However, delivering stem cells through this route poses a challenge since their viability must be preserved and cells can be swept away by nasal mucus. Earlier attempts at intranasal cell therapy have shown low efficiency, but still hold promise to the future. The hydrogels designed for this study can provide stem cells with a biocompatible environment and adhesion to the nasal atrium, easing the successful migration of viable cells to the brain., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Author(s). Published by Elsevier Ltd.. All rights reserved.)
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- 2024
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21. Leptin haploinsufficiency exerts sex-dependent partial protection in SOD1 G93A mice by reducing inflammatory pathways in the adipose tissue.
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Fernández-Beltrán LC, Ali Z, Larrad-Sanz A, Lopez-Carbonero JI, Godoy-Corchuelo JM, Jimenez-Coca I, Garcia-Toledo I, Bentley L, Gomez-Pinedo U, Matias-Guiu JA, Gil-Moreno MJ, Matias-Guiu J, and Corrochano S
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- Animals, Female, Humans, Male, Mice, Adipose Tissue metabolism, Disease Models, Animal, Haploinsufficiency, Leptin metabolism, Mice, Transgenic, Spinal Cord metabolism, Superoxide Dismutase metabolism, Superoxide Dismutase-1 genetics, Superoxide Dismutase-1 metabolism, Amyotrophic Lateral Sclerosis metabolism
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Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by significant metabolic disruptions, including weight loss and hypermetabolism in both patients and animal models. Leptin, an adipose-derived hormone, displays altered levels in ALS. Genetically reducing leptin levels (Lepob/+) to maintain body weight improved motor performance and extended survival in female SOD1G93A mice, although the exact molecular mechanisms behind these effects remain elusive. Here, we corroborated the sexual dimorphism in circulating leptin levels in ALS patients and in SOD1G93A mice. We reproduced a previous strategy to generate a genetically deficient leptin SOD1G93A mice (SOD1G93ALepob/+) and studied the transcriptomic profile in the subcutaneous adipose tissue and the spinal cord. We found that leptin deficiency reduced the inflammation pathways activated by the SOD1G93A mutation in the adipose tissue, but not in the spinal cord. These findings emphasize the importance of considering sex-specific approaches in metabolic therapies and highlight the role of leptin in the systemic modulation of ALS by regulating immune responses outside the central nervous system., (© 2024. The Author(s).)
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- 2024
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22. Mesenchymal Stem Cell-Based Therapies in the Post-Acute Neurological COVID Syndrome: Current Landscape and Opportunities.
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León-Moreno LC, Reza-Zaldívar EE, Hernández-Sapiéns MA, Villafaña-Estarrón E, García-Martin M, Ojeda-Hernández DD, Matias-Guiu JA, Gomez-Pinedo U, Matias-Guiu J, and Canales-Aguirre AA
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- Humans, SARS-CoV-2, Post-Acute COVID-19 Syndrome, Central Nervous System, COVID-19 therapy, Mesenchymal Stem Cells physiology
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One of the main concerns related to SARS-CoV-2 infection is the symptoms that could be developed by survivors, known as long COVID, a syndrome characterized by persistent symptoms beyond the acute phase of the infection. This syndrome has emerged as a complex and debilitating condition with a diverse range of manifestations affecting multiple organ systems. It is increasingly recognized for affecting the Central Nervous System, in which one of the most prevalent manifestations is cognitive impairment. The search for effective therapeutic interventions has led to growing interest in Mesenchymal Stem Cell (MSC)-based therapies due to their immunomodulatory, anti-inflammatory, and tissue regenerative properties. This review provides a comprehensive analysis of the current understanding and potential applications of MSC-based interventions in the context of post-acute neurological COVID-19 syndrome, exploring the underlying mechanisms by which MSCs exert their effects on neuroinflammation, neuroprotection, and neural tissue repair. Moreover, we discuss the challenges and considerations specific to employing MSC-based therapies, including optimal delivery methods, and functional treatment enhancements.
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- 2023
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23. Hippocampal subfield abnormalities and biomarkers of pathologic brain changes: from SARS-CoV-2 acute infection to post-COVID syndrome.
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Díez-Cirarda M, Yus-Fuertes M, Sanchez-Sanchez R, Gonzalez-Rosa JJ, Gonzalez-Escamilla G, Gil-Martínez L, Delgado-Alonso C, Gil-Moreno MJ, Valles-Salgado M, Cano-Cano F, Ojeda-Hernandez D, Gomez-Ruiz N, Oliver-Mas S, Benito-Martín MS, Jorquera M, de la Fuente S, Polidura C, Selma-Calvo B, Arrazola J, Matias-Guiu J, Gomez-Pinedo U, and Matias-Guiu JA
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- Humans, Brain diagnostic imaging, Brain pathology, Hippocampus pathology, Atrophy, Syndrome, Biomarkers, SARS-CoV-2, COVID-19 pathology
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Background: Cognitive deficits are among the main disabling symptoms in COVID-19 patients and post-COVID syndrome (PCS). Within brain regions, the hippocampus, a key region for cognition, has shown vulnerability to SARS-CoV-2 infection. Therefore, in vivo detailed evaluation of hippocampal changes in PCS patients, validated on post-mortem samples of COVID-19 patients at the acute phase, would shed light into the relationship between COVID-19 and cognition., Methods: Hippocampal subfields volume, microstructure, and perfusion were evaluated in 84 PCS patients and compared to 33 controls. Associations with blood biomarkers, including glial fibrillary acidic protein (GFAP), myelin oligodendrocyte glycoprotein (MOG), eotaxin-1 (CCL11) and neurofilament light chain (NfL) were evaluated. Besides, biomarker immunodetection in seven hippocampal necropsies of patients at the acute phase were contrasted against eight controls., Findings: In vivo analyses revealed that hippocampal grey matter atrophy is accompanied by altered microstructural integrity, hypoperfusion, and functional connectivity changes in PCS patients. Hippocampal structural and functional alterations were related to cognitive dysfunction, particularly attention and memory. GFAP, MOG, CCL11 and NfL biomarkers revealed alterations in PCS, and showed associations with hippocampal volume changes, in selective hippocampal subfields. Moreover, post mortem histology showed the presence of increased GFAP and CCL11 and reduced MOG concentrations in the hippocampus in post-mortem samples at the acute phase., Interpretation: The current results evidenced that PCS patients with cognitive sequalae present brain alterations related to cognitive dysfunction, accompanied by a cascade of pathological alterations in blood biomarkers, indicating axonal damage, astrocyte alterations, neuronal injury, and myelin changes that are already present from the acute phase., Funding: Nominative Grant FIBHCSC 2020 COVID-19. Department of Health, Community of Madrid. Instituto de Salud Carlos III through the project INT20/00079, co-funded by European Regional Development Fund "A way to make Europe" (JAMG). Instituto de Salud Carlos III (ISCIII) through Sara Borrell postdoctoral fellowship Grant No. CD22/00043) and co-funded by the European Union (MDC). Instituto de Salud Carlos III through a predoctoral contract (FI20/000145) (co-funded by European Regional Development Fund "A way to make Europe") (MVS). Fundación para el Conocimiento Madri+d through the project G63-HEALTHSTARPLUS-HSP4 (JAMG, SOM)., Competing Interests: Declaration of interests The authors declare that they have no competing interests., (Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.)
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- 2023
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24. Editorial: Current advances in genetic presentations of dementia and aging, volume II.
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Xu Y, Gomez-Pinedo U, Liu J, Hong D, and Xu J
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Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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- 2023
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25. Editorial: Current advances in genetic dementia and aging.
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Xu Y, Hong D, Gomez-Pinedo U, Liu J, and Xu J
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Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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- 2022
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26. Editorial: COVID-19 in CNS and PNS: Basic and Clinical Focus on the Mechanisms of Infection and New Tools for the Therapeutic Approach.
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Matias-Guiu J, Matias-Guiu JA, Garrido C, Pimienta G, Reyes PF, Baig AM, and Gomez-Pinedo U
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Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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- 2022
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27. Biocompatibility of ferulic/succinic acid-grafted chitosan hydrogels for implantation after brain injury: A preliminary study.
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Ojeda-Hernández DD, Gomez-Pinedo U, Hernández-Sapiéns MA, Canales-Aguirre AA, Espinosa-Andrews H, Matias-Guiu J, González-García Y, and Mateos-Díaz JC
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- Animals, Biocompatible Materials pharmacology, Hydrogels, Rats, Rats, Wistar, Succinic Acid, Brain Injuries drug therapy, Chitosan
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Nowadays it is known that neural cells are capable of regenerating after brain injury, but their success highly depends on the local environment, including the presence of a biological structure to support cell proliferation and restore the lost tissue. Different chitosan-based biomaterials have been employed in response to this necessity. We hypothesized that hydrogels made of antioxidant compounds functionalizing chitosan could provide a suitable environment to home new cells and offer a way to achieve brain repair. In this work, the implantation of functionalized chitosan biomaterials in a brain injury animal model was evaluated. The injury consisted of mechanical damage applied to the cerebral cortex of Wistar rats followed by the implantation of four different chitosan-based biomaterials. After 15 and 30 days, animals underwent magnetic resonance imaging, then they were sacrificed, and the brain tissue was analyzed by immunohistochemistry. The proliferation of microglia and astrocytes increased at the lesion zone, showing differences between the evaluated biomaterials. Also, cell nuclei were seen inside the biomaterials, indicating cell migration and biodegradation. Chitosan-based hydrogels are able to fill in the tissue cavity and bare cells for the endogenous restoration process. The addition of ferulic and succinic acid to the chitosan structure increases this capacity and decreases the inflammatory reaction to the implant., (Copyright © 2020 Elsevier B.V. All rights reserved.)
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- 2021
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28. Is the brain a reservoir organ for SARS-CoV2?
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Gomez-Pinedo U, Matias-Guiu J, Sanclemente-Alaman I, Moreno-Jimenez L, Montero-Escribano P, and Matias-Guiu JA
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- Angiotensin-Converting Enzyme 2 metabolism, Brain metabolism, Humans, Receptors, Coronavirus metabolism, Virus Internalization, Brain virology, COVID-19 virology, SARS-CoV-2 physiology
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- 2020
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29. SARS-CoV-2 as a Potential Trigger of Neurodegenerative Diseases.
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Gomez-Pinedo U, Matias-Guiu J, Sanclemente-Alaman I, Moreno-Jimenez L, Montero-Escribano P, and Matias-Guiu JA
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- Aging, Betacoronavirus, COVID-19, Humans, SARS-CoV-2, Coronavirus Infections, Neurodegenerative Diseases, Pandemics, Pneumonia, Viral, Severe acute respiratory syndrome-related coronavirus
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- 2020
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30. Potential of Chitosan and Its Derivatives for Biomedical Applications in the Central Nervous System.
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Ojeda-Hernández DD, Canales-Aguirre AA, Matias-Guiu J, Gomez-Pinedo U, and Mateos-Díaz JC
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It is well known that the central nervous system (CNS) has a limited regenerative capacity and that many therapeutic molecules cannot cross the blood brain barrier (BBB). The use of biomaterials has emerged as an alternative to overcome these limitations. For many years, biomedical applications of chitosan have been studied due to its remarkable biological properties, biocompatibility, and high versatility. Moreover, the interest in this biomaterial for CNS biomedical implementation has increased because of its ability to cross the BBB, mucoadhesiveness, and hydrogel formation capacity. Several chitosan-based biomaterials have been applied with promising results as drug, cell and gene delivery vehicles. Moreover, their capacity to form porous scaffolds and to bear cells and biomolecules has offered a way to achieve neural regeneration. Therefore, this review aims to bring together recent works that highlight the potential of chitosan and its derivatives as adequate biomaterials for applications directed toward the CNS. First, an overview of chitosan and its derivatives is provided with an emphasis on the properties that favor different applications. Second, a compilation of works that employ chitosan-based biomaterials for drug delivery, gene therapy, tissue engineering, and regenerative medicine in the CNS is presented. Finally, the most interesting trends and future perspectives of chitosan and its derivatives applications in the CNS are shown., (Copyright © 2020 Ojeda-Hernández, Canales-Aguirre, Matias-Guiu, Gomez-Pinedo and Mateos-Díaz.)
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- 2020
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31. Should we expect neurological symptoms in the SARS-CoV-2 epidemic?
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Matías-Guiu J, Gomez-Pinedo U, Montero-Escribano P, Gomez-Iglesias P, Porta-Etessam J, and Matias-Guiu JA
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- Animals, Betacoronavirus, COVID-19, Coronavirus Infections complications, Disease Models, Animal, Humans, Mice, Pandemics, Pneumonia, Viral complications, SARS-CoV-2, Central Nervous System virology, Coronavirus Infections physiopathology, Pneumonia, Viral physiopathology
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Introduction: There is growing evidence that SARS-CoV-2 can gain access to the central nervous system (CNS). We revise the literature on coronavirus infection of the CNS associated with neurological diseases., Development: Neurological symptoms were rarely reported in the SARS-CoV and MERS-CoV epidemics, although isolated cases were described. There are also reports of cases of neurological symptoms associated with CoV-OC43 and CoV-229E infection. The presence of neurological lesions, especially demyelinating lesions in the mouse hepatitis virus model, may explain the mechanisms by which coronaviruses enter the CNS, particularly those related with the immune response. This may explain the presence of coronavirus in patients with multiple sclerosis. We review the specific characteristics of SARS-CoV-2 and address the question of whether the high number of cases may be associated with greater CNS involvement., Conclusion: Although neurological symptoms are not frequent in coronavirus epidemics, the high number of patients with SARS-CoV-2 infection may explain the presence of the virus in the CNS and increase the likelihood of early- or delayed-onset neurological symptoms. Follow-up of patients affected by the SARS-CoV-2 epidemic should include careful assessment of the CNS., (Copyright © 2020 Sociedad Española de Neurología. Publicado por Elsevier España, S.L.U. All rights reserved.)
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- 2020
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32. Vitamin D increases remyelination by promoting oligodendrocyte lineage differentiation.
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Gomez-Pinedo U, Cuevas JA, Benito-Martín MS, Moreno-Jiménez L, Esteban-Garcia N, Torre-Fuentes L, Matías-Guiu JA, Pytel V, Montero P, and Matías-Guiu J
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- Animals, Cell Differentiation drug effects, Cell Differentiation physiology, Cell Lineage drug effects, Male, Multiple Sclerosis therapy, Neural Stem Cells physiology, Rats, Rats, Wistar, Treatment Outcome, Vitamins metabolism, Vitamins pharmacology, Oligodendroglia physiology, Remyelination drug effects, Remyelination physiology, Vitamin D metabolism, Vitamin D pharmacology
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Introduction: Several experimental studies have suggested the potential remyelinating effects of vitamin D (VitD) supplements regardless of the presence of VitD deficiency. This study aims to analyze neurogenesis in a model of toxic demyelination in order to evaluate the effects of VitD on demyelination and remyelination., Material and Methods: We used 24 male Wistar rats that had received surgical lesions to the corpus callosum and were injected with lysolecithin. Rats were divided into three groups: Group 1 included eight rats with lesions to the corpus callosum but not lysolecithin injections (sham group), group 2 included eight rats with lesions to the corpus callosum that were injected with lysolecithin (lysolecithin group), and group 3 included eight rats with lesions that were injected with lysolecithin and received VitD (VitD group). We analyzed neurogenesis both in the subventricular zone and at the lesion site., Results: Administration of VitD promotes the proliferation and differentiation of neural stem cells in the subventricular zone and the migration of these cells to the lesion site in the corpus callosum; these cells subsequently differentiate into oligodendrocyte lineage cells and produce myelin basic protein. This phenomenon was not caused by microglial activation, which was less marked in rats receiving VitD. Megalin expression did not increase at the lesion site, which suggests that VitD is internalized by other mechanisms., Conclusion: Our results support the hypothesis that regardless of the presence of VitD deficiency, treatment with VitD may contribute to remyelination by promoting the proliferation of oligodendrocyte precursor cells., (© 2019 The Authors. Brain and Behavior published by Wiley Periodicals, Inc.)
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- 2020
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33. Mesenchymal stem cell-derived exosomes promote neurogenesis and cognitive function recovery in a mouse model of Alzheimer's disease.
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Reza-Zaldivar EE, Hernández-Sapiéns MA, Gutiérrez-Mercado YK, Sandoval-Ávila S, Gomez-Pinedo U, Márquez-Aguirre AL, Vázquez-Méndez E, Padilla-Camberos E, and Canales-Aguirre AA
- Abstract
Studies have shown that mesenchymal stem cell-derived exosomes can enhance neural plasticity and improve cognitive impairment. The purpose of this study was to investigate the effects of mesenchymal stem cell-derived exosomes on neurogenesis and cognitive capacity in a mouse model of Alzheimer's disease. Alzheimer's disease mouse models were established by injection of beta amyloid 1-42 aggregates into dentate gyrus bilaterally. Morris water maze and novel object recognition tests were performed to evaluate mouse cognitive deficits at 14 and 28 days after administration. Afterwards, neurogenesis in the subventricular zone was determined by immunofluorescence using doublecortin and PSA-NCAM antibodies. Results showed that mesenchymal stem cells-derived exosomes stimulated neurogenesis in the subventricular zone and alleviated beta amyloid 1-42-induced cognitive impairment, and these effects are similar to those shown in the mesenchymal stem cells. These findings provide evidence to validate the possibility of developing cell-free therapeutic strategies for Alzheimer's disease. All procedures and experiments were approved by Institutional Animal Care and Use Committee (CICUAL) (approval No. CICUAL 2016-011) on April 25, 2016., Competing Interests: None
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- 2019
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34. Clinical or neuroimaging profiles in the assessment of genetic variants associated with neurodegenerative diseases.
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Matías-Guiu J, Torre-Fuentes L, Gomez-Pinedo U, and Matías-Guiu JA
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- Brain, Gait, Humans, Neuroimaging, Neurodegenerative Diseases, Parkinson Disease
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- 2019
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35. News in multiple sclerosis: Remyelination as a therapeutic target.
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Matías-Guiu J, Gomez-Pinedo U, and Matias-Guiu JA
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- Humans, Immunologic Factors pharmacology, Multiple Sclerosis diagnosis, Multiple Sclerosis physiopathology, Peripheral Nervous System Agents pharmacology, Immunologic Factors therapeutic use, Multiple Sclerosis drug therapy, Peripheral Nervous System Agents therapeutic use, Remyelination drug effects
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- 2017
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36. Cellular changes in motor neuron cell culture produced by cytotoxic cerebrospinal fluid from patients with amyotrophic lateral sclerosis.
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Gomez-Pinedo U, Yáñez M, Matías-Guiu J, Galán L, Guerrero-Sola A, Benito-Martin MS, Vela A, Arranz-Tagarro JA, and García AG
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- Animals, Cells, Cultured, Cerebrospinal Fluid chemistry, Cytotoxins pharmacology, Humans, Motor Neurons cytology, Motor Neurons metabolism, Rats, Amyotrophic Lateral Sclerosis cerebrospinal fluid, Cerebrospinal Fluid metabolism, Glutamic Acid pharmacology, Motor Neurons drug effects
- Abstract
Introduction: The neurotoxic effects of cerebrospinal fluid (CSF) from patients with amyotrophic lateral sclerosis (ALS) have been reported by various authors who have attributed this neurotoxicity to the glutamate in CSF-ALS., Material and Methods: Cultures of rat embryonic cortical neurons were exposed to CSF from ALS patients during an incubation period of 24 hours. Optical microscopy was used to compare cellular changes to those elicited by exposure to 100μm glutamate, and confocal microscopy was used to evaluate immunohistochemistry for caspase-3, TNFα, and peripherin., Results: In the culture exposed to CSF-ALS, we observed cells with nuclear fragmentation and scarce or null structural modifications to the cytoplasmic organelles or to plasma membrane maintenance. This did not occur in the culture exposed to glutamate. The culture exposed to CSF-ALS also demonstrated increases in caspase-3, TNFα, and in peripherin co-locating with caspase-3, but not with TNFα, suggesting that TNFα may play an early role in the process of apoptosis., Conclusions: CFS-ALS cytotoxicity is not related to glutamate. It initially affects the nucleus without altering the cytoplasmic membrane. It causes cytoplasmic apoptosis that involves an increase in caspase-3 co-located with peripherin, which is also overexpressed., (Copyright © 2013 Sociedad Española de Neurología. Published by Elsevier Espana. All rights reserved.)
- Published
- 2014
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37. The adult macaque spinal cord central canal zone contains proliferative cells and closely resembles the human.
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Alfaro-Cervello C, Cebrian-Silla A, Soriano-Navarro M, Garcia-Tarraga P, Matías-Guiu J, Gomez-Pinedo U, Molina Aguilar P, Alvarez-Buylla A, Luquin MR, and Garcia-Verdugo JM
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- Adult, Age Factors, Aged, Aged, 80 and over, Animals, Epithelial Cells physiology, Female, Humans, Macaca, Macaca fascicularis, Male, Species Specificity, Spinal Canal ultrastructure, Spinal Cord ultrastructure, Cell Proliferation physiology, Spinal Canal cytology, Spinal Canal physiology, Spinal Cord cytology, Spinal Cord physiology
- Abstract
The persistence of proliferative cells, which could correspond to progenitor populations or potential cells of origin for tumors, has been extensively studied in the adult mammalian forebrain, including human and nonhuman primates. Proliferating cells have been found along the entire ventricular system, including around the central canal, of rodents, but little is known about the primate spinal cord. Here we describe the central canal cellular composition of the Old World primate Macaca fascicularis via scanning and transmission electron microscopy and immunohistochemistry and identify central canal proliferating cells with Ki67 and newly generated cells with bromodeoxyuridine incorporation 3 months after the injection. The central canal is composed of uniciliated, biciliated, and multiciliated ependymal cells, astrocytes, and neurons. Multiciliated ependymal cells show morphological characteristics similar to multiciliated ependymal cells from the lateral ventricles, and uniciliated and biciliated ependymal cells display cilia with large, star-shaped basal bodies, similar to the Ecc cells described for the rodent central canal. Here we show that ependymal cells with one or two cilia, but not multiciliated ependymal cells, proliferate and give rise to new ependymal cells that presumably remain in the macaque central canal. We found that the infant and adult human spinal cord contains ependymal cell types that resemble those present in the macaque. Interestingly, a wide hypocellular layer formed by bundles of intermediate filaments surrounded the central canal both in the monkey and in the human, being more prominent in the stenosed adult human central canal., (Copyright © 2013 Wiley Periodicals, Inc.)
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- 2014
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38. GFP immunogold staining, from light to electron microscopy, in mammalian cells.
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Sirerol-Piquer MS, Cebrián-Silla A, Alfaro-Cervelló C, Gomez-Pinedo U, Soriano-Navarro M, and Verdugo JM
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- Animals, Humans, Fluorescent Dyes, Green Fluorescent Proteins, Immunohistochemistry methods, Staining and Labeling methods
- Abstract
GFP has emerged as an important reporter for monitoring gene expression, protein localization, cell transformation and cell lineage. The development of GFP as a marker in many different biological systems has emphasized the need to image GFP at high resolution. GFP immunogold labeling with colloidal gold particles becomes essential for electron microscopy (EM) ultrastructural detection. Because of the small size, colloidal gold particles require silver enhancement, a procedure to increase the size of the particle as well as gold toning to stabilize the silver layer. GFP preembedding immunogold staining enables high quality cellular-ultrastructural EM analysis mainly for two reasons, on one hand it allows adequate fixation for EM analysis maintaining GFP antigenicity, on the other hand it also enables the epoxy resins inclusion after immunogold staining. Both of them help to preserve better the ultrastructure. However GFP immunogold staining presents some drawbacks, such as the progressive decrease in immunogold labeling with tissue depth. Special attention must be taken when using GFP-tagged protein, since the fusion could interfere with their localization and function. In this review we provide a detailed protocol of the GFP immunogold staining, their main applications for EM and possible troubles., (Copyright © 2011 Elsevier Ltd. All rights reserved.)
- Published
- 2012
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39. Therapeutic effects of hMAPC and hMSC transplantation after stroke in mice.
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Mora-Lee S, Sirerol-Piquer MS, Gutiérrez-Pérez M, Gomez-Pinedo U, Roobrouck VD, López T, Casado-Nieto M, Abizanda G, Rabena MT, Verfaille C, Prósper F, and García-Verdugo JM
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- Adult Stem Cells cytology, Animals, Brain blood supply, Brain pathology, Cell Movement, Cell Survival, Humans, Infarction, Middle Cerebral Artery pathology, Infarction, Middle Cerebral Artery physiopathology, Infarction, Middle Cerebral Artery surgery, Infarction, Middle Cerebral Artery therapy, Male, Mice, Multipotent Stem Cells cytology, Neovascularization, Physiologic, Stroke pathology, Stroke physiopathology, Stroke surgery, Adult Stem Cells transplantation, Mesenchymal Stem Cell Transplantation, Multipotent Stem Cells transplantation, Stroke therapy
- Abstract
Stroke represents an attractive target for stem cell therapy. Although different types of cells have been employed in animal models, a direct comparison between cell sources has not been performed. The aim of our study was to assess the effect of human multipotent adult progenitor cells (hMAPCs) and human mesenchymal stem cells (hMSCs) on endogenous neurogenesis, angiogenesis and inflammation following stroke. BALB/Ca-RAG 2(-/-) γC(-/-) mice subjected to FeCl(3) thrombosis mediated stroke were intracranially injected with 2 × 10(5) hMAPCs or hMSCs 2 days after stroke and followed for up to 28 days. We could not detect long-term engraftment of either cell population. However, in comparison with PBS-treated animals, hMSC and hMAPC grafted animals demonstrated significantly decreased loss of brain tissue. This was associated with increased angiogenesis, diminished inflammation and a glial-scar inhibitory effect. Moreover, enhanced proliferation of cells in the subventricular zone (SVZ) and survival of newly generated neuroblasts was observed. Interestingly, these neuroprotective effects were more pronounced in the group of animals treated with hMAPCs in comparison with hMSCs. Our results establish cell therapy with hMAPCs and hMSCs as a promising strategy for the treatment of stroke.
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- 2012
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40. Subventricular zone in motor neuron disease with frontotemporal dementia.
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Galan L, Gomez-Pinedo U, Vela-Souto A, Guerrero-Sola A, Barcia JA, Gutierrez AR, Martinez-Martinez A, Jiménez MS, García-Verdugo JM, and Matias-Guiu J
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- Aged, Amyotrophic Lateral Sclerosis complications, Amyotrophic Lateral Sclerosis diagnosis, Amyotrophic Lateral Sclerosis pathology, Female, Frontotemporal Dementia complications, Frontotemporal Dementia diagnosis, Humans, Motor Neuron Disease diagnosis, Motor Neuron Disease etiology, Nerve Degeneration diagnosis, Nerve Degeneration etiology, Neural Stem Cells cytology, Neural Stem Cells metabolism, Neurogenesis physiology, Telencephalon cytology, Telencephalon metabolism, Frontotemporal Dementia pathology, Motor Neuron Disease pathology, Nerve Degeneration pathology
- Abstract
Investigate how the subventricular proliferation and organisation is modified in a patient with FTLD-ALS. We studied the subventricular zone (SVZ) of a patient with FTLD-ALS immunohistochemical and histologically. We found an increase of Ki-67 positive cells and neuroblast in the subventricular zone, suggesting an activation of proliferating activity in response to FTD-ALS. This proliferation can act as a compensatory mechanism for rapid neuronal death and its modulation could provide a new therapeutic pathway in ALS. These results suggest a modification of neurogenesis in FTD-ALS., (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)
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- 2011
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41. Neuronal activity drives localized blood-brain-barrier transport of serum insulin-like growth factor-I into the CNS.
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Nishijima T, Piriz J, Duflot S, Fernandez AM, Gaitan G, Gomez-Pinedo U, Verdugo JM, Leroy F, Soya H, Nuñez A, and Torres-Aleman I
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- Action Potentials drug effects, Action Potentials physiology, Analysis of Variance, Animals, Biophysics methods, Blood-Brain Barrier drug effects, Blood-Brain Barrier ultrastructure, Body Temperature drug effects, Cells, Cultured, Central Nervous System drug effects, Coculture Techniques, Digoxigenin metabolism, Drug Interactions, Electric Stimulation methods, Endothelial Cells metabolism, Endothelial Cells ultrastructure, Enzyme-Linked Immunosorbent Assay methods, Excitatory Amino Acid Antagonists pharmacology, Functional Laterality, Glutamic Acid pharmacology, Humans, Immunoprecipitation methods, Insulin-Like Growth Factor I pharmacology, Low Density Lipoprotein Receptor-Related Protein-1 metabolism, Matrix Metalloproteinase 9 metabolism, Microdialysis methods, Microscopy, Immunoelectron methods, Nerve Tissue Proteins metabolism, Neural Pathways, Neuroglia drug effects, Neuroglia physiology, Neurons drug effects, Neurons ultrastructure, Protein Transport drug effects, Rats, Rats, Wistar, Receptor, IGF Type 1 metabolism, Regional Blood Flow drug effects, Regional Blood Flow physiology, Time Factors, Vibrissae innervation, Blood-Brain Barrier metabolism, Central Nervous System metabolism, Insulin-Like Growth Factor I metabolism, Neurons physiology
- Abstract
Upon entry into the central nervous system (CNS), serum insulin-like growth factor-1 (IGF-I) modulates neuronal growth, survival, and excitability. Yet mechanisms that trigger IGF-I entry across the blood-brain barrier remain unclear. We show that neuronal activity elicited by electrical, sensory, or behavioral stimulation increases IGF-I input in activated regions. Entrance of serum IGF-I is triggered by diffusible messengers (i.e., ATP, arachidonic acid derivatives) released during neurovascular coupling. These messengers stimulate matrix metalloproteinase-9, leading to cleavage of the IGF binding protein-3 (IGFBP-3). Cleavage of IGFBP-3 allows the passage of serum IGF-I into the CNS through an interaction with the endothelial transporter lipoprotein related receptor 1. Activity-dependent entrance of serum IGF-I into the CNS may help to explain disparate observations such as proneurogenic effects of epilepsy, rehabilitatory effects of neural stimulation, and modulatory effects of blood flow on brain activity., (2010 Elsevier Inc. All rights reserved.)
- Published
- 2010
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42. Hyperammonemia induces neuroinflammation that contributes to cognitive impairment in rats with hepatic encephalopathy.
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Rodrigo R, Cauli O, Gomez-Pinedo U, Agusti A, Hernandez-Rabaza V, Garcia-Verdugo JM, and Felipo V
- Subjects
- Animals, Anti-Inflammatory Agents, Non-Steroidal pharmacology, Bile Ducts surgery, Brain immunology, Brain pathology, Cell Movement, Cognition Disorders immunology, Cognition Disorders pathology, Cognition Disorders prevention & control, Cognition Disorders psychology, Disease Models, Animal, Hepatic Encephalopathy immunology, Hepatic Encephalopathy pathology, Hepatic Encephalopathy prevention & control, Hepatic Encephalopathy psychology, Hyperammonemia drug therapy, Hyperammonemia immunology, Hyperammonemia pathology, Hyperammonemia psychology, Ibuprofen pharmacology, Inflammation drug therapy, Inflammation immunology, Inflammation pathology, Inflammation psychology, Inflammation Mediators metabolism, Learning, Ligation, Male, Microglia immunology, Microglia pathology, Motor Activity, Quaternary Ammonium Compounds, Rats, Rats, Wistar, Behavior, Animal drug effects, Cognition drug effects, Cognition Disorders etiology, Hepatic Encephalopathy etiology, Hyperammonemia complications, Inflammation etiology
- Abstract
Background & Aims: Hyperammonemia and inflammation cooperate to induce neurological alterations in hepatic encephalopathy. Recent studies in animal models suggest that chronic hyperammonemia and neuroinflammation impair learning ability by the same mechanism. Chronic hyperammonemia might induce inflammatory factors in the brain that impair cognitive function. We sought to determine whether hyperammonemia itself induces neuroinflammation, whether ammonia-induced neuroinflammation mediates cognitive impairment, and whether neuroinflammation also occurs in rats with bile duct ligation (BDL rats)-a model of chronic liver injury that results in hyperammonemia and hepatic encephalopathy., Methods: Chronic moderate hyperammonemia was induced by feeding male Wistar rats an ammonium-containing diet or performing BDL. Rats that received a standard diet or a sham operation were used as controls. Neuroinflammation was assessed by measuring activation of microglia and inflammatory factors. Brain samples were collected from hyperammonemic and BDL rats; microglial activation was determined by immunohistochemistry and quantification of inflammatory markers (ie, inducible nitric oxide synthase, interleukin-1beta, and prostaglandin E2). Learning ability and motor activity were assessed in hyperammonemic and BDL rats given ibuprofen as an anti-inflammatory agent., Results: Chronic moderate hyperammonemia or BDL activated the microglia, especially in cerebellum; increased inducible nitric oxide synthase, interleukin-1beta, and prostaglandin E2 levels; and impaired cognitive and motor function, compared with controls. Ibuprofen reduced microglial activation and restored cognitive and motor functions in the hyperammonemic and BDL rats., Conclusions: Chronic hyperammonemia is sufficient to induce microglial activation and neuroinflammation; these contribute to the cognitive and motor alterations that occur during hepatic encephalopathy., (Copyright (c) 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.)
- Published
- 2010
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43. Ultrastructural analysis of guided nerve regeneration using progesterone- and pregnenolone-loaded chitosan prostheses.
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Chávez-Delgado ME, Gomez-Pinedo U, Feria-Velasco A, Huerta-Viera M, Castañeda SC, Toral FA, Parducz A, Anda SL, Mora-Galindo J, and García-Estrada J
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- Animals, Drug Delivery Systems, Facial Nerve pathology, Male, Microscopy, Electron, Polymers chemistry, Progesterone chemistry, Rabbits, Regeneration, Steroids metabolism, Time Factors, Biocompatible Materials chemistry, Chitosan chemistry, Nerve Regeneration, Neurons ultrastructure, Pregnenolone metabolism, Progesterone metabolism
- Abstract
Recently, numerous guide chambers for the treatment of injured nerves made up of different biomaterials have been designed, capable of hosting living cells or carrying neurotrophic or neuroactive substances to be directly released to the injured tissue. In this study, chitosan prostheses containing neurosteroids (progesterone and pregnenolone) were used for bridging a 10-mm gap in the rabbit facial nerve. Gas chromatography was used to quantify neurosteroid content in the prostheses prior to and after subcutaneous implantation at different periods of up to 60 days. The regeneration of the nerve fibers were evaluated at 15 and 45 days after axotomy by means of ultrastructural morphometric analysis. Different nerve fibers regenerative patterns were seen depending the groups studied and the analyzed stages. At 15 days after axotomy, the newly regenerating tissue revealed Schwann cells holding nonmyelinated nerve fiber bundles in an incipient and organized regenerative pattern. At 45 days, the regenerating tissue showed myelinated nerve fibers of different sizes, shapes, and myelin sheath thickness. Although the regeneration of the nerve fibers under neurosteroid treatment showed statistically significant differences in comparison with vehicle regenerated tissue, progesterone-loaded chitosan prostheses produced the best guided nerve regeneration response. These findings indicate that chitosan prostheses allowed regeneration of nerve fibers in their lumen, and when containing neurosteroids produced a faster guided nerve regeneration acting as a long-lasting release delivery vehicle., (Copyright 2005 Wiley Periodicals, Inc.)
- Published
- 2005
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