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Localization of Fas antigen mRNA induced in postischemic murine forebrain by in situ hybridization
T Matsuyama1, R Hata, Y Yamamoto
1Fifth Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Japan.
Abstract:
The expression of mRNA for the Fas antigen, a membrane-associated protein mediating apoptosis, was localized by in situ hybridization histochemistry in murine brains following 30 min of global cerebral ischemia. Six hours following the ischemia, many labeled cells were detected anew throughout the brain. The hybridization was seen in the small neural cells and in the cells along the walls of the ventricles and vessels, and became undetectable 24 h following the ischemia. These results suggest that the Fas antigen is expressed in the neuron, glia and periventricular cells of the post-ischemic brain.
Insights
Global cerebral ischemia rapidly induces Fas antigen expression in mouse brain cells, including neurons and glia. This expression is transient, appearing by 6 hours and disappearing by 24 hours post-ischemia.
Area of Science:
- Neuroscience
- Cell Biology
Background:
- Apoptosis, or programmed cell death, plays a role in brain injury.
- The Fas antigen is a key mediator of apoptosis.
Purpose of the Study:
- To investigate the expression of Fas antigen mRNA in the brain after global cerebral ischemia.
- To determine which cell types in the brain express Fas antigen following ischemic events.
Main Methods:
- In situ hybridization histochemistry was used to localize Fas antigen mRNA.
- Murine brains were analyzed at various time points after 30 minutes of global cerebral ischemia.
Main Results:
- Fas antigen mRNA was detected in various brain cells 6 hours after ischemia.
- Labeled cells included neurons, glia, and cells lining ventricles and vessels.
- Fas antigen expression was undetectable 24 hours after ischemia.
Conclusions:
- Fas antigen is transiently expressed in neurons, glia, and periventricular cells following global cerebral ischemia.
- This suggests a role for Fas-mediated apoptosis in the post-ischemic brain.