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Updated: Jul 17, 2026
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Modeling Stroke in Mice: Focal Cortical Lesions by Photothrombosis
Published on: May 6, 2021
Proteomics of experimental stroke in mice
Melanie Föcking1, Michael Besselmann, Thorsten Trapp
1Laboratory for Molecular Pathology and Neuroregeneration, Institute for Transplantation Diagnostics and Cell Therapeutics, Medical Center, Heinrich-Heine-University, Moorenstr. 5, Building 14.80, 40225 Diisseldorf, Germany.
Acta Neurobiologiae Experimentalis
|February 3, 2007
Summary
This study investigated protein changes in mouse brains after transient focal ischemia. Significant protein alterations occurred in both affected and unaffected hemispheres, revealing complex injury pathways.
Area of Science:
- Neuroscience
- Proteomics
- Ischemic Stroke Research
Background:
- Transient focal ischemia is a major cause of brain injury.
- Understanding protein level changes is crucial for identifying therapeutic targets.
Purpose of the Study:
- To analyze proteomic changes in the brain following transient focal ischemia.
- To investigate the temporal regulation of proteins in both ischemic and non-ischemic hemispheres.
Main Methods:
- Multi-Western blot analysis of over 400 proteins.
- Mouse model of transient focal ischemia using middle cerebral artery (MCA) occlusion.
- Analysis at 1 hour ischemia and 3, 12 hours post-reperfusion.
Main Results:
- Up to 45% of proteins were significantly altered (≥1.5 fold change) in the ipsilateral hemisphere post-ischemia.
- Approximately 50% of proteins were regulated in the non-ischemic hemisphere, indicating contralateral involvement.
- Temporal regulation patterns of specific proteins were identified.
Conclusions:
- Proteomic analysis provides deeper insights into ischemic brain damage than transcriptomic studies.
- Ischemic stroke involves complex, multi-pathway injury mechanisms affecting both hemispheres.
- This study may help identify key mediators of ischemic brain injury for future therapeutic strategies.
