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21 results on '"Abiega, Oihane"'

1. Astrocyte-targeted gene delivery of interleukin 2 specifically increases brain-resident regulatory T cell numbers and protects against pathological neuroinflammation

Author

Yshii, Lidia, Pasciuto, Emanuela, Bielefeld, Pascal, Mascali, Loriana, Lemaitre, Pierre, Marino, Marika, Dooley, James, Kouser, Lubna, Verschoren, Stijn, Lagou, Vasiliki, Kemps, Hannelore, Gervois, Pascal, de Boer, Antina, Burton, Oliver T., Wahis, Jérôme, Verhaert, Jens, Tareen, Samar H. K., Roca, Carlos P., Singh, Kailash, Whyte, Carly E., Kerstens, Axelle, Callaerts-Vegh, Zsuzsanna, Poovathingal, Suresh, Prezzemolo, Teresa, Wierda, Keimpe, Dashwood, Amy, Xie, Junhua, Van Wonterghem, Elien, Creemers, Eline, Aloulou, Meryem, Gsell, Willy, Abiega, Oihane, Munck, Sebastian, Vandenbroucke, Roosmarijn E., Bronckaers, Annelies, Lemmens, Robin, De Strooper, Bart, Van Den Bosch, Ludo, Himmelreich, Uwe, Fitzsimons, Carlos P., Holt, Matthew G., and Liston, Adrian

Published
2022
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3. Astrocyte-targeted gene delivery of interleukin 2 specifically increases brain-resident regulatory T cell numbers and protects against pathological neuroinflammation

Author

Yshii, Lidia, primary, Pasciuto, Emanuela, additional, Bielefeld, Pascal, additional, Mascali, Loriana, additional, Lemaitre, Pierre, additional, Marino, Marika, additional, Dooley, James, additional, Kouser, Lubna, additional, Verschoren, Stijn, additional, Lagou, Vasiliki, additional, Kemps, Hannelore, additional, Gervois, Pascal, additional, de Boer, Antina, additional, Burton, Oliver T., additional, Wahis, Jérôme, additional, Verhaert, Jens, additional, Tareen, Samar, additional, Roca, Carlos P., additional, Singh, Kailash, additional, Whyte, Carly E., additional, Kerstens, Axelle, additional, Callaerts-Vegh, Zsuzsanna, additional, Poovathingal, Suresh, additional, Prezzemolo, Teresa, additional, Wierda, Keimpe, additional, Dashwood, Amy, additional, Xie, Junhua, additional, Van Wonterghem, Elien, additional, Creemers, Eline, additional, Aloulou, Meryem, additional, Gsell, Willy, additional, Abiega, Oihane, additional, Munck, Sebastian, additional, Vandenbroucke, Roosmarijn E., additional, Bronckaers, Annelies, additional, Lemmens, Robin, additional, De Strooper, Bart, additional, Van Den Bosch, Ludo, additional, Himmelreich, Uwe, additional, Fitzsimons, Carlos P., additional, Holt, Matthew G., additional, and Liston, Adrian, additional

Published
2022
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5. An emerging role for microglia in stress‐effects on memory

Author

Sanguino‐Gómez, Jeniffer, primary, Buurstede, Jacobus C., additional, Abiega, Oihane, additional, Fitzsimons, Carlos P., additional, Lucassen, Paul J., additional, Eggen, Bart J. L., additional, Lesuis, Sylvie L., additional, Meijer, Onno C., additional, and Krugers, Harm J., additional

Published
2021
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6. An emerging role for microglia in stress‐effects on memory.

Author

Sanguino‐Gómez, Jeniffer, Buurstede, Jacobus C., Abiega, Oihane, Fitzsimons, Carlos P., Lucassen, Paul J., Eggen, Bart J. L., Lesuis, Sylvie L., Meijer, Onno C., and Krugers, Harm J.

Subjects
MICROGLIA, MEMORY disorders, NEUROPLASTICITY, MEMORY, IMMUNE response
Abstract

Stressful experiences evoke, among others, a rapid increase in brain (nor)epinephrine (NE) levels and a slower increase in glucocorticoid hormones (GCs) in the brain. Microglia are key regulators of neuronal function and contain receptors for NE and GCs. These brain cells may therefore potentially be involved in modulating stress effects on neuronal function and learning and memory. In this review, we discuss that stress induces (1) an increase in microglial numbers as well as (2) a shift toward a pro‐inflammatory profile. These microglia have (3) impaired crosstalk with neurons and (4) disrupted glutamate signaling. Moreover, microglial immune responses after stress (5) alter the kynurenine pathway through metabolites that impair glutamatergic transmission. All these effects could be involved in the impairments in memory and in synaptic plasticity caused by (prolonged) stress, implicating microglia as a potential novel target in stress‐related memory impairments. [ABSTRACT FROM AUTHOR]

Published
2022
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8. Microglial phagocytosis dysfunction is related to local neuronal activity in a genetic model of epilepsy

Author

Sierra-Torre, Virginia, Plaza-Zabala, Ainhoa, Bonifazi, Paolo, Abiega, Oihane, Díaz-Aparicio, Irune, Tegelberg, Saara, Lehesjoki, Anna-Elina, Valero, Jorge, and Sierra, Amanda

Subjects
0303 health sciences, Microglia, Phagocytosis, Excitotoxicity, Inflammation, Progressive myoclonus epilepsy, Biology, medicine.disease_cause, medicine.disease, Cell biology, Subgranular zone, 03 medical and health sciences, 0302 clinical medicine, medicine.anatomical_structure, Cystatin B, Genetic model, medicine, medicine.symptom, 030217 neurology & neurosurgery, 030304 developmental biology
Abstract

Microglial phagocytosis of apoptotic cells is an essential component of the brain regenerative response in neurodegenerative diseases. Phagocytosis is very efficient in physiological conditions, as well as during apoptotic challenge induced by excitotoxicity or inflammation, but is impaired in mouse and human mesial temporal lobe epilepsy (MTLE). Here we extend our studies to a genetic model of progressive myoclonus epilepsy type 1 (EPM1) in mice lacking cystatin B (CSTB), an inhibitor of cysteine proteases involved in lysosomal proteolysis. We first demonstrated that microglial phagocytosis was impaired in the hippocampus in Cstb knock-out (KO) mice when seizures arise and hippocampal atrophy begins, at 1 month of age. To test if this blockage was related to the lack of Cstb in microglia, we used an in vitro model of phagocytosis and siRNAs to acutely reduce Cstb expression but we found no significant effect in the phagocytosis of apoptotic cells. We then tested whether seizures were involved in the phagocytosis impairment, similar to MTLE, and analyzed Cstb KO mice before seizures begin, at postnatal day 14. Here, phagocytosis impairment was restricted to the granule neuron layer but not to the subgranular zone, where there are no active neurons. Furthermore, we observed apoptotic cells (both phagocytosed and not phagocytosed) in Cstb deficient mice at close proximity to active, cFos+ neurons and used mathematical modeling to demonstrate that the physical relationship between apoptotic cells and cFos+ neurons was specific for Cstb KO mice. These results suggest a complex crosstalk between apoptosis, phagocytosis and neuronal activity, hinting that local neuronal activity could be related to phagocytosis dysfunction in Cstb KO mice. Overall, this data suggest that phagocytosis impairment is an early feature of hippocampal damage in epilepsy and opens novel therapeutic approaches for epileptic patients based on targeting microglial phagocytosis.

Published
2020

12. Microglia Actively Remodel Adult Hippocampal Neurogenesis through the Phagocytosis Secretome

Author

Diaz-Aparicio, Irune, primary, Paris, Iñaki, additional, Sierra-Torre, Virginia, additional, Plaza-Zabala, Ainhoa, additional, Rodríguez-Iglesias, Noelia, additional, Márquez-Ropero, Mar, additional, Beccari, Sol, additional, Huguet, Paloma, additional, Abiega, Oihane, additional, Alberdi, Elena, additional, Matute, Carlos, additional, Bernales, Irantzu, additional, Schulz, Angela, additional, Otrokocsi, Lilla, additional, Sperlagh, Beata, additional, Happonen, Kaisa E., additional, Lemke, Greg, additional, Maletic-Savatic, Mirjana, additional, Valero, Jorge, additional, and Sierra, Amanda, additional

Published
2020
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13. Microglia actively remodels adult hippocampal neurogenesis through the phagocytosis secretome

Author

Diaz-Aparicio, Irune, primary, Paris, Iñaki, additional, Sierra-Torre, Virginia, additional, Plaza-Zabala, Ainhoa, additional, Rodríguez-Iglesias, Noelia, additional, Márquez-Ropero, Mar, additional, Beccari, Sol, additional, Abiega, Oihane, additional, Alberdi, Elena, additional, Matute, Carlos, additional, Bernales, Irantzu, additional, Schulz, Angela, additional, Otrokocsi, Lilla, additional, Sperlagh, Beata, additional, Happonen, Kaisa E., additional, Lemke, Greg, additional, Maletic-Savatic, Mirjana, additional, Valero, Jorge, additional, and Sierra, Amanda, additional

Published
2019
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15. Correction: Neuronal Hyperactivity Disturbs ATP Microgradients, Impairs Microglial Motility, and Reduces Phagocytic Receptor Expression Triggering Apoptosis/Microglial Phagocytosis Uncoupling

Author

Abiega, Oihane, Beccari, Sol, Diaz-Aparicio, Irune, Nadjar, Agnes, Layé, Sophie, Leyrolle, Quentin, Gómez-Nicola, Diego, Domercq, María, Pérez-Samartín, Alberto, Sánchez-Zafra, Víctor, Paris, Iñaki, Valero, Jorge, Savage, Julie C., Hui, Chin-Wai, Tremblay, Marie-Ève, Deudero, Juan J. P., Brewster, Amy L., Anderson, Anne E., Zaldumbide, Laura, Galbarriatu, Lara, Marinas, Ainhoa, Vivanco, Maria dM., Matute, Carlos, Maletic-Savatic, Mirjana, Encinas, Juan M., and Sierra, Amanda

Subjects
Correction
Published
2016

16. Neuronal Hyperactivity Disturbs ATP Microgradients, Impairs Microglial Motility, and Reduces Phagocytic Receptor Expression Triggering Apoptosis/Microglial Phagocytosis Uncoupling

Author

Abiega, Oihane, primary, Beccari, Sol, additional, Diaz-Aparicio, Irune, additional, Nadjar, Agnes, additional, Layé, Sophie, additional, Leyrolle, Quentin, additional, Gómez-Nicola, Diego, additional, Domercq, María, additional, Pérez-Samartín, Alberto, additional, Sánchez-Zafra, Víctor, additional, Paris, Iñaki, additional, Valero, Jorge, additional, Savage, Julie C., additional, Hui, Chin-Wai, additional, Tremblay, Marie-Ève, additional, Deudero, Juan J. P., additional, Brewster, Amy L., additional, Anderson, Anne E., additional, Zaldumbide, Laura, additional, Galbarriatu, Lara, additional, Marinas, Ainhoa, additional, Vivanco, Maria dM., additional, Matute, Carlos, additional, Maletic-Savatic, Mirjana, additional, Encinas, Juan M., additional, and Sierra, Amanda, additional

Published
2016
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19. Neuronal Hyperactivity Accelerates Depletion of Neural Stem Cells and Impairs Hippocampal Neurogenesis

Author

Sierra, Amanda, primary, Martín-Suárez, Soraya, additional, Valcárcel-Martín, Roberto, additional, Pascual-Brazo, Jesús, additional, Aelvoet, Sarah-Ann, additional, Abiega, Oihane, additional, Deudero, Juan J., additional, Brewster, Amy L., additional, Bernales, Irantzu, additional, Anderson, Anne E., additional, Baekelandt, Veerle, additional, Maletić-Savatić, Mirjana, additional, and Encinas, Juan M., additional

Published
2015
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21. Clearing the corpses: regulatory mechanisms, novel tools, and therapeutic potential of harnessing microglial phagocytosis in the diseased brain.

Author

Diaz-Aparicio I, Beccari S, Abiega O, and Sierra A

Abstract

Apoptosis is a widespread phenomenon that occurs in the brain in both physiological and pathological conditions. Dead cells must be quickly removed to avoid the further toxic effects they exert in the parenchyma, a process executed by microglia, the brain professional phagocytes. Although phagocytosis is critical to maintain tissue homeostasis, it has long been either overlooked or indirectly assessed based on microglial morphology, expression of classical activation markers, or engulfment of artificial phagocytic targets in vitro . Nevertheless, these indirect methods present several limitations and, thus, direct observation and quantification of microglial phagocytosis is still necessary to fully grasp its relevance in the diseased brain. To overcome these caveats and obtain a comprehensive, quantitative picture of microglial phagocytosis we have developed a novel set of parameters. These parameters have allowed us to identify the different strategies utilized by microglia to cope with apoptotic challenges induced by excitotoxicity or inflammation. In contrast, we discovered that in mouse and human epilepsy microglia failed to find and engulf apoptotic cells, resulting in accumulation of debris and inflammation. Herein, we advocate that the efficiency of microglial phagocytosis should be routinely tested in neurodegenerative and neurological disorders, in order to determine the extent to which it contributes to apoptosis and inflammation found in these conditions. Finally, our findings point towards enhancing microglial phagocytosis as a novel therapeutic strategy to control tissue damage and inflammation, and accelerate recovery in brain diseases., Competing Interests: Conflicts of Interest: None declared.

Published
2016
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