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A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model
Published on: June 4, 2021
In situ deposition of complement in human acute brain ischaemia
E D Pedersen1, E M Løberg, E Vege
1Faculty of Medicine, Institute of Immunology, Rikshospitalet University Hospital, University of Oslo, Oslo, Norway. elena.pedersen@rr-research.no
Scandinavian Journal of Immunology
|May 15, 2009
Summary
Complement activation and reduced regulators in human brain ischemia suggest a key role in stroke damage. This study investigated complement
Area of Science:
- Neuroscience
- Immunology
Background:
- Animal models suggest complement system involvement in ischemic stroke.
- Limited data exist on complement's role in human stroke pathology.
Purpose of the Study:
- To investigate complement activation in human brain following acute ischemia.
- To assess the expression of complement regulators in ischemic brain tissue.
Main Methods:
- Indirect immunohistochemical staining on human brain tissue from stroke patients and controls.
- Detection of complement components (C1q, C3c, C4d, C9) and regulators (CD59, CD55).
Main Results:
- Classical complement pathway activation indicated by C1q, C3c, C4d deposition in lesions.
- C9, C-reactive protein, and IgM found in necrotic areas.
- Reduced expression of complement regulators CD59 and CD55 in ischemic lesions compared to normal brain.
Conclusions:
- Increased complement component deposition and decreased regulator expression contribute to ischemic brain tissue damage.
- The complement system is implicated in human stroke pathogenesis.
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