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Up-regulation of macrophage migration-inhibitory factor expression after compression-induced spinal cord injury in
Masao Koda1, Yutaka Nishio, Masayuki Hashimoto
1Department of Environmental Medical Science, Chiba University Graduate School of Medicine, Japan. masaokoda@faculty.chiba-u.jp
Abstract:
Macrophage migration inhibitory factor (MIF) is a multipotential protein that acts as a pro-inflammatory cytokine, pituitary hormone, immunoregulator, and mitogen. To elucidate function of MIF in spinal cord injury, we examined expression of MIF after compression-induced spinal cord injury using Northern blot analysis, in situ hybridization and immunohistochemistry. The MIF mRNA was up-regulated in injured spinal cord, peaking 3 days after injury shown by Northern blot analysis. In situ hybridization revealed up-regulation of MIF in microglia accumulating in the lesion epicenter 3 days after injury and astrocytes around the cystic cavity 1 week after injury. Double staining showed co-localization of MIF and tomato lectin in the lesioned site, indicating that microglia accumulating to the lesion epicenter express MIF. The time course of MIF expression is different from that of previous reports about cytokine expression peaking at earlier time points; thus, it is unlikely that MIF acts as a pro-inflammatory factor in the present study. The MIF may contribute to proliferation of astrocytes around the lesioned site in spinal cord injury because of its cell proliferation-promoting property.
Insights
Macrophage migration inhibitory factor (MIF) expression increases after spinal cord injury, primarily in microglia and astrocytes. This suggests MIF may promote astrocyte proliferation rather than inflammation post-injury.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Macrophage migration inhibitory factor (MIF) is a pleiotropic protein with roles in inflammation, immunity, and cell proliferation.
- Understanding the role of MIF in the complex cascade of events following spinal cord injury (SCI) is crucial for therapeutic development.
Purpose of the Study:
- To investigate the expression patterns and cellular localization of MIF in a compression-induced rat spinal cord injury model.
- To elucidate the potential function of MIF in the context of SCI, differentiating its role from acute inflammatory responses.
Main Methods:
- Compression-induced SCI model in rats.
- Northern blot analysis to assess MIF mRNA expression levels over time.
- In situ hybridization and immunohistochemistry to determine the cellular source and localization of MIF.
- Double staining techniques (MIF with tomato lectin) to identify expressing cell types.
Main Results:
- MIF mRNA expression was significantly upregulated in the injured spinal cord, peaking at 3 days post-injury.
- In situ hybridization revealed MIF expression in microglia at the lesion epicenter (3 days post-injury) and astrocytes surrounding the cystic cavity (1 week post-injury).
- Double staining confirmed MIF expression in microglia, co-localizing with tomato lectin.
Conclusions:
- The temporal expression profile of MIF in SCI differs from typical acute pro-inflammatory cytokines, suggesting a non-inflammatory role in this context.
- MIF's presence in microglia and astrocytes, coupled with its known mitogenic properties, indicates a potential role in promoting astrocyte proliferation and tissue repair following SCI.
