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Published on: September 4, 2013
Increased Expression of Interferon-Induced Transmembrane 3 (IFITM3) in Stroke and Other Inflammatory Conditions in
Elisabeth Harmon1, Andrea Doan1, Jesus Bautista-Garrido1
1Department of Neurology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
Abstract:
Microglia, the resident innate immune cells of the brain, become more highly reactive with aging and diseased conditions. In collaboration with other cell types in brains, microglia can contribute both to worsened outcome following stroke or other neurodegenerative diseases and to the recovery process by changing their phenotype toward reparative microglia. Recently, IFITM3 (a member of the "interferon-inducible transmembrane" family) has been revealed as a molecular mediator between amyloid pathology and neuroinflammation. Expression of IFITM3 in glial cells, especially microglia following stroke, is not well described. Here, we present evidence that ischemic stroke causes an increase in IFITM3 expression along with increased microglial activation marker genes in aged brains. To further validate the induction of IFITM3 in post-stroke brains, primary microglia and microglial-like cells were exposed to a variety of inflammatory conditions, which significantly induced IFITM3 as well as other inflammatory markers. These findings suggest the critical role of IFITM3 in inducing inflammation. Our findings on the expression of IFITM3 in microglia and in aged brains following stroke could establish the basic foundations for the role of IFITM3 in a variety of neurodegenerative diseases, particularly those that are prevalent or enhanced in the aged brain.
Insights
Interferon-inducible transmembrane protein 3 (IFITM3) expression increases in aged brain microglia after ischemic stroke. This suggests IFITM3 plays a key role in neuroinflammation and age-related neurodegenerative diseases.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Microglia, the brain's immune cells, become reactive with age and disease.
- Microglia influence both neurodegeneration and recovery after brain injury.
- Interferon-inducible transmembrane protein 3 (IFITM3) is implicated in amyloid pathology and neuroinflammation.
Purpose of the Study:
- To investigate IFITM3 expression in microglia following ischemic stroke, particularly in aged brains.
- To understand the role of IFITM3 in microglial activation and neuroinflammation.
Main Methods:
- Examined IFITM3 expression in aged mouse brains post-ischemic stroke.
- Analyzed microglial activation markers alongside IFITM3.
- Exposed primary microglia and microglial-like cells to inflammatory stimuli to assess IFITM3 induction.
Main Results:
- Ischemic stroke increased IFITM3 expression in aged brains.
- Microglial activation markers were also elevated post-stroke.
- In vitro inflammatory conditions significantly induced IFITM3 and other inflammatory markers in microglia.
Conclusions:
- IFITM3 expression is upregulated in microglia following ischemic stroke, especially in aged brains.
- IFITM3 appears to play a critical role in mediating inflammation.
- Findings provide a foundation for IFITM3's role in age-related neurodegenerative diseases.
