Related Experiment Video
Updated: Sep 25, 2026
An Integrated Method for Photothrombotic Stroke Modeling and In Vivo Optrode Recording of Neuronal and Astrocytic Activity in Behaving Mice
Published on: May 29, 2026
Dynamic expression of p38beta MAPK in neurons and astrocytes after transient focal ischemia
Chun Shu Piao1, Young-Mi Yu, Pyung-Lim Han
1Department of Anatomy, Inha University School of Medicine, 7-241 Shinheung-dong, Jung-Gu, Inchon 400-712, South Korea.
Abstract:
Here we report the dynamically regulated expression of p38beta MAPK isoform in specific subsets of cells in postischemic brain. The activity of p38beta MAPK in the postischemic brain revealed biphasic induction at 30 min and 4 days after 1 h MCAO. During the early surge period, p38beta MAPK was preferentially localized in the nucleus and dendrites of neurons in the future infarction area, while during the delayed surge p38beta MAPK was heavily induced in reactive astrocytes in penumbra. The temporally and spatially regulated pattern of p38beta MAPK expression in the postischemic brain suggests distinct roles of p38beta MAPK in neuronal death and in the astrocyte activation.
Insights
This study reveals the dynamic expression of p38beta mitogen-activated protein kinase (MAPK) in the postischemic brain. Its distinct cellular localization suggests varied roles in neuronal death and astrocyte activation following stroke.
Area of Science:
- Neuroscience
- Molecular Biology
- Pathology
Background:
- Ischemic stroke triggers complex cellular responses in the brain.
- Mitogen-activated protein kinases (MAPKs) are implicated in cellular signaling pathways following injury.
Purpose of the Study:
- To investigate the expression pattern of the p38beta MAPK isoform in the brain after ischemia.
- To elucidate the temporal and spatial roles of p38beta MAPK in postischemic neuronal and glial responses.
Main Methods:
- Middle cerebral artery occlusion (MCAO) model in rodents to induce focal ischemia.
- Immunohistochemistry to detect p38beta MAPK localization in neuronal and glial cells.
- Analysis of protein expression at different time points post-ischemia.
Main Results:
- Biphasic induction of p38beta MAPK activity observed at 30 minutes and 4 days after 1-hour MCAO.
- Early surge: p38beta MAPK localized in neurons (nucleus, dendrites) in the infarction area.
- Delayed surge: p38beta MAPK heavily induced in reactive astrocytes within the penumbra.
Conclusions:
- The expression of p38beta MAPK is dynamically regulated in specific cell types post-ischemia.
- Distinct temporal and spatial localization suggests differential roles in neuronal injury and astrocyte reactivity.
- p38beta MAPK may play a dual role in the complex cascade of events following ischemic stroke.
