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Updated: Dec 25, 2025
A Model for Encephalomyosynangiosis Treatment after Middle Cerebral Artery Occlusion-Induced Stroke in Mice
Published on: June 22, 2022
EMMPRIN/CD147 plays a detrimental role in clinical and experimental ischemic stroke
Anthony Patrizz1, Sarah J Doran2, Anjali Chauhan1
1The University of Texas Health Science Center at Houston and the McGovern Medical School, Houston, TX 77030, USA.
Background:
Ischemic stroke is a devastating disease, often resulting in death or permanent neurological deficits. EMMPRIN/CD147 is a plasma membrane protein that induces the production of matrix metalloproteinases (MMPs), which contribute to secondary damage after stroke by disrupting the blood brain barrier (BBB) and facilitating peripheral leukocyte infiltration into the brain.
Results:
CD147 surface expression increased significantly after stroke on infiltrating leukocytes, astrocytes and endothelial cells, but not on resident microglia. Inhibition of CD147 reduced MMP levels, decreased ischemic damage, and improved functional, cognitive and histological outcomes after experimental ischemic stroke in both young and aged mice. In stroke patients, high levels of serum CD147 24 hours after stroke predicted poor functional outcome at 12 months. Brain CD147 levels were correlated with MMP-9 and secondary hemorrhage in post-mortem samples from stroke patients.
Conclusions:
Acute inhibition of CD147 decreases levels of MMP-9, limits tissue loss, and improves long-term cognitive outcomes following experimental stroke in aged mice. High serum CD147 correlates with poor outcomes in stroke patients. This study identifies CD147 as a novel, clinically relevant target in ischemic stroke.
Insights
Targeting EMMPRIN/CD147, a protein involved in ischemic stroke damage, significantly improved outcomes in mice and correlated with poor patient prognosis. This highlights CD147 as a promising therapeutic target for stroke.
Area of Science:
- Neuroscience
- Immunology
- Biochemistry
Background:
- Ischemic stroke causes severe neurological deficits and death.
- EMMPRIN/CD147, a plasma membrane protein, drives matrix metalloproteinase (MMP) production.
- MMPs disrupt the blood-brain barrier (BBB) and promote brain inflammation post-stroke.
Purpose of the Study:
- To investigate the role of EMMPRIN/CD147 in ischemic stroke.
- To evaluate CD147 as a potential therapeutic target for stroke.
- To assess the correlation between CD147 levels and stroke outcomes in patients.
Main Methods:
- Examined CD147 expression on brain cells and leukocytes after stroke in mice.
- Inhibited CD147 in experimental stroke models (young and aged mice).
- Measured MMP levels, brain damage, and functional recovery.
- Correlated serum CD147 levels with clinical outcomes in stroke patients.
Main Results:
- CD147 expression increased on infiltrating leukocytes, astrocytes, and endothelial cells post-stroke.
- CD147 inhibition reduced MMP levels, ischemic damage, and improved outcomes in mice.
- High serum CD147 levels in patients predicted poor functional recovery at 12 months.
- Brain CD147 levels correlated with MMP-9 and secondary hemorrhage in patients.
Conclusions:
- Acute CD147 inhibition limits tissue loss and improves cognitive function post-stroke.
- Elevated serum CD147 is a biomarker for poor stroke outcomes.
- CD147 represents a novel and clinically relevant therapeutic target for ischemic stroke.
