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Non-invasive Imaging and Analysis of Cerebral Ischemia in Living Rats Using Positron Emission Tomography with 18F-FDG
Published on: December 28, 2014
VEGF and flt. Expression time kinetics in rat brain infarct
Z Kovács1, K Ikezaki, K Samoto
1Department of Neurosurgery, Kyushu University Faculty of Medicine, Fukuoka, Japan.
Stroke
|October 1, 1996
Summary
Vascular endothelial growth factor (VEGF) and its receptor (flt) are expressed in the ischemic brain, indicating their role in the healing process of brain infarcts.
Area of Science:
- Neuroscience
- Molecular Biology
- Pathology
Background:
- Vascular endothelial growth factor (VEGF) is a potent mitogen for endothelial cells and is upregulated by hypoxia.
- VEGF is implicated in angiogenesis and hyperpermeability, making it a potential factor in infarcts.
Purpose of the Study:
- To investigate the chronological expression of the VEGF/flt system in experimental cerebral infarction.
- To elucidate the cellular sources and localization of VEGF and its receptor during infarct development.
Main Methods:
- A middle cerebral artery occlusion model was used in rats.
- VEGF expression was quantified using Western blotting.
- Immunohistochemistry was employed to analyze the chronological expression of the VEGF/flt system from 3 hours to 3 weeks post-infarction.
Main Results:
- VEGF and its receptor flt were exclusively detected in the ischemic brain.
- VEGF immunoreactivity was observed in macrophages, neurons, and glial cells over time.
- Both VEGF and flt were found in endothelial cells, correlating with angiogenesis.
Conclusions:
- Macrophages, neurons, and glial cells are sources of VEGF in the ischemic brain.
- The VEGF receptor flt is induced in endothelial cells during infarct angiogenesis.
- The VEGF/flt system plays a significant role in the brain infarct healing process.
