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Updated: Jan 4, 2026
Intravital Imaging of Axonal Interactions with Microglia and Macrophages in a Mouse Dorsal Column Crush Injury
Published on: November 23, 2014
Macrophage migration inhibitory factor derived from spinal cord is involved in activation of macrophages following
Yingjie Wang1, Sumei Wei1, Honghua Song1
1Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-innovation Center of Neuroregeneration, Nantong University, Nantong, China.
Abstract:
Macrophages and their initiation of acute inflammation have been defined to be functionally important in tissue repair and regeneration. In injury-induced production of macrophage migration inhibitory factor (MIF), which has been described as a pleiotropic protein that participates in multiple cellular and biologic processes, it is unknown whether it is involved in the regulation of macrophage events during the epimorphic regeneration. In the model of gecko tail amputation, the protein levels of gecko MIF (gMIF) have been determined to be significantly increased in the nerve cells of the spinal cord in association with the recruitment of macrophages to the lesion site. gMIF has been shown to interact with the CD74 receptor to promote the migration of macrophages through activation of Ras homolog gene family member A and to trigger inflammatory responses through MAPK signaling pathways. The determination of microsphere phagocytosis also indicated that gMIF could enhance macrophage phagocytosis. gMIF-mediated recruitment and activation of macrophages have been found to be necessary for gecko tail regeneration, as evidenced by the depletion of macrophages using clodronate liposomes. The results present a novel function of MIF during the epimorphic regeneration, which is beneficial for insights into its pleiotropic property.-Wang, Y., Wei, S., Song, H., Zhang, X., Wang, W., Du, N., Song, T., Liang, H., Chen, X., Wang, Y. Macrophage migration inhibitory factor derived from spinal cord is involved in activation of macrophages following gecko tail amputation.
Insights
Macrophage migration inhibitory factor (MIF) from spinal cord nerves aids gecko tail regeneration by recruiting and activating macrophages. This discovery reveals a new role for MIF in epimorphic regeneration.
Area of Science:
- Regenerative Biology
- Immunology
- Molecular Biology
Background:
- Macrophages and acute inflammation are crucial for tissue repair and regeneration.
- Macrophage migration inhibitory factor (MIF) is a pleiotropic protein involved in various cellular processes.
- The role of MIF in regulating macrophage activity during epimorphic regeneration remains unclear.
Purpose of the Study:
- To investigate the involvement of gecko MIF (gMIF) in macrophage recruitment and activation during epimorphic regeneration.
- To elucidate the molecular mechanisms by which gMIF influences macrophage behavior.
- To determine the necessity of gMIF-mediated macrophage activity for successful tail regeneration in geckos.
Main Methods:
- Gecko tail amputation model.
- Quantification of gMIF protein levels in spinal cord nerve cells.
- Assessment of macrophage recruitment to the lesion site.
- Investigation of gMIF interaction with CD74 receptor.
- Analysis of Ras homolog gene family member A and MAPK signaling pathways.
- Microsphere phagocytosis assays.
- Macrophage depletion using clodronate liposomes.
Main Results:
- gMIF protein levels significantly increased in spinal cord nerve cells post-amputation, correlating with macrophage recruitment.
- gMIF interacts with CD74, promoting macrophage migration via Ras homolog gene family member A activation and triggering inflammation through MAPK pathways.
- gMIF enhances macrophage phagocytosis.
- Depletion of macrophages abrogated gMIF-mediated tail regeneration, indicating necessity.
Conclusions:
- Spinal cord-derived gMIF plays a critical role in macrophage recruitment and activation during gecko tail regeneration.
- gMIF's novel function in epimorphic regeneration highlights its multifaceted biological properties.
- This study provides new insights into the complex mechanisms governing regeneration and the pleiotropic nature of MIF.
