In vitro P38MAPK inhibition in aged astrocytes decreases reactive astrocytes, inflammation and increases nutritive capacity after oxygen-glucose deprivation

dc.contributor
Institut Català de la Salut
dc.contributor
[Revuelta M] Department for Neonatology, Charité University Medical Center, Berlin, Germany. Cellular Oncology Group, Biodonostia Health Research Institute, San Sebastian, Spain. [Elicegui A] Department for Neonatology, Charité University Medical Center, Berlin, Germany. Laboratori de Recerca Neurovascular, Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. [Scheuer T, Endesfelder S, Bührer C] Department for Neonatology, Charité University Medical Center, Berlin, Germany. [Moreno-Cugnon L] Cellular Oncology Group, Biodonostia Health Research Institute, San Sebastian, Spain
dc.contributor
Vall d'Hebron Barcelona Hospital Campus
dc.contributor.author
Revuelta, Miren
dc.contributor.author
Elicegui Aguirre, Amaia
dc.contributor.author
Scheuer, Till
dc.contributor.author
Endesfelder, Stefanie
dc.contributor.author
Bührer, Christoph
dc.contributor.author
Moreno-Cugnon, Leire
dc.date.accessioned
2025-10-24T08:49:59Z
dc.date.available
2025-10-24T08:49:59Z
dc.date.issued
2022-04-04T11:52:00Z
dc.date.issued
2022-04-04T11:52:00Z
dc.date.issued
2021-02-09
dc.identifier
Revuelta M, Elicegui A, Scheuer T, Endesfelder S, Bührer C, Moreno-Cugnon L, et al. In vitro P38MAPK inhibition in aged astrocytes decreases reactive astrocytes, inflammation and increases nutritive capacity after oxygen-glucose deprivation. Aging. 2021 Feb 9;13(5):6346–58.
dc.identifier
1945-4589
dc.identifier
https://hdl.handle.net/11351/7291
dc.identifier
10.18632/aging.202651
dc.identifier
33563843
dc.identifier
000629616300010
dc.identifier.uri
http://hdl.handle.net/11351/7291
dc.description.abstract
Envelliment; Astròcits; P38MAPK
dc.description.abstract
Envejecimiento; Astrocitos; P38MAPK
dc.description.abstract
Ageing; Atrocytes; P38MAPK
dc.description.abstract
Proper astroglial functioning is essential for the development and survival of neurons and oligodendroglia under physiologic and pathological circumstances. Indeed, malfunctioning of astrocytes represents an important factor contributing to brain injury. However, the molecular pathways of this astroglial dysfunction are poorly defined. In this work we show that aging itself can drastically perturb astrocyte viability with an increase of inflammation, cell death and astrogliosis. Moreover, we demonstrate that oxygen glucose deprivation (OGD) has a higher impact on nutritive loss in aged astrocytes compared to young ones, whereas aged astrocytes have a higher activity of the anti-oxidant systems. P38MAPK signaling has been identified to be upregulated in neurons, astrocytes and microglia after ischemic stroke. By using a pharmacological p38α specific inhibitor (PH-797804), we show that p38MAPK pathway has an important role in aged astrocytes for inflammatory and oxidative stress responses with the subsequent cell death that occurs after OGD.
dc.description.abstract
Deutsche Forschungsgemeinschaft (SCHE 2078/2-1). Förderverein für frühgeborene Kinder an der Charité e.V. Basque Government Postdoc (2017_1_0095).
dc.format
application/pdf
dc.language
eng
dc.publisher
Impact Journals
dc.relation
Aging;13(5)
dc.relation
https://doi.org/10.18632/aging.202651
dc.rights
Attribution 4.0 International
dc.rights
http://creativecommons.org/licenses/by/4.0/
dc.rights
info:eu-repo/semantics/openAccess
dc.source
Scientia
dc.subject
Dany cerebral
dc.subject
Astròcits - Metabolisme
dc.subject
DISEASES::Nervous System Diseases::Central Nervous System Diseases::Brain Diseases::Brain Injuries
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ANATOMY::Cells::Neuroglia::Astrocytes
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Other subheadings::Other subheadings::Other subheadings::/metabolism
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ENFERMEDADES::enfermedades del sistema nervioso::enfermedades del sistema nervioso central::enfermedades cerebrales::lesiones encefálicas
dc.subject
ANATOMÍA::células::neuroglía::astrocitos
dc.subject
Otros calificadores::Otros calificadores::Otros calificadores::/metabolismo
dc.title
In vitro P38MAPK inhibition in aged astrocytes decreases reactive astrocytes, inflammation and increases nutritive capacity after oxygen-glucose deprivation
dc.type
info:eu-repo/semantics/article
dc.type
info:eu-repo/semantics/publishedVersion


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