Research Paper Volume 13, Issue 5 pp 6346—6358
In vitro P38MAPK inhibition in aged astrocytes decreases reactive astrocytes, inflammation and increases nutritive capacity after oxygen-glucose deprivation
- 1 Department for Neonatology, Charité University Medical Center, Berlin 13353, Germany
- 2 Cellular Oncology Group, Biodonostia Health Research Institute, Paseo Doctor Begiristain, San Sebastian 20014, Spain
- 3 Neurovascular Research Laboratory, Vall d’Hebron Institute of Research, Barcelona 08035, Spain
- 4 IKERBASQUE, Basque Foundation for Science, Bilbao 48013, Spain
- 5 CIBERfes, Madrid 28029, Spain
Received: July 22, 2020 Accepted: December 18, 2020 Published: February 9, 2021https://doi.org/10.18632/aging.202651
How to Cite
Copyright: © 2021 Revuelta et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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.