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Updated: May 28, 2026
08:22
Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model
Published on: June 20, 2025
The CEBPB-AP-1 (JunB/Fos) Axis Drives Neuroinflammation and Microglial Dysfunction Via TNF Signaling in Ischemic
Kun Liang1, Shuangshuang Lu2, Weihao Shi1
1Department of Vascular Surgery, Huashan Hospital, Fudan University, Shanghai, China.
Inflammation
|May 26, 2026
Summary
The transcription factor CEBPB drives neuroinflammation after ischemic stroke by activating the AP-1 complex in microglia. Inhibiting this pathway reduces inflammation, neuronal damage, and improves functional recovery, offering a new therapeutic target.
Area of Science:
- Neuroscience
- Immunology
- Molecular Biology
Background:
- Ischemic stroke induces neuroinflammation, involving microglia with complex roles in damage and repair.
- Mechanisms controlling microglial activation and polarization in stroke are not fully understood.
Purpose of the Study:
- To identify key molecular regulators of microglial pro-inflammatory responses in ischemic stroke.
- To investigate the role of the transcription factor CEBPB and the AP-1 complex in stroke-induced neuroinflammation.
Main Methods:
- Transcriptomic profiling of microglia from mice subjected to transient focal cerebral ischemia (tFCI).
- Investigated the binding of CEBPB to the Fos promoter.
- Utilized a selective AP-1 inhibitor (T-5224) in vitro and in vivo models of tFCI.
Main Results:
- CEBPB was identified as a key regulator of AP-1 (JunB-Fos) complex formation and pro-inflammatory gene expression in microglia.
- CEBPB directly activates the Fos promoter, leading to increased IL-1β and TNF-α production.
- AP-1 inhibition shifted microglia to an anti-inflammatory phenotype, reduced neuroinflammation, neuronal apoptosis, and improved functional outcomes in tFCI mice.
Conclusions:
- The CEBPB/AP-1 axis is a critical driver of neuroinflammation in ischemic stroke.
- Targeting the CEBPB/AP-1 pathway represents a promising therapeutic strategy for stroke treatment.
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