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Published on: September 5, 2016
Brain miffed by macrophage migration inhibitory factor
Nic E Savaskan1, Günter Fingerle-Rowson, Michael Buchfelder
1Department of Neurosurgery, University of Erlangen-Nuremberg, Schwabachanlage 6, 91054 Erlangen, Germany.
Abstract:
Macrophage migration inhibitory factor (MIF) is a cytokine which also exhibits enzymatic properties like oxidoreductase and tautomerase. MIF plays a pivotal role in innate and acquired immunity as well as in the neuroendocrine axis. Since it is involved in the pathogenesis of acute and chronic inflammation, neoangiogenesis, and cancer, MIF and its signaling components are considered suitable targets for therapeutic intervention in several fields of medicine. In neurodegenerative and neurooncological diseases, MIF is a highly relevant, but still a hardly investigated mediator. MIF operates via intracellular protein-protein interaction as well as in CD74/CXCR2/CXCR4 receptor-mediated pathways to regulate essential cellular systems such as redox balance, HIF-1, and p53-mediated senescence and apoptosis as well as multiple signaling pathways. Acting as an endogenous glucocorticoid antagonist, MIF thus represents a relevant resistance gene in brain tumor therapies. Alongside this dual action, a functional homolog-annotated D-dopachrome tautomerase/MIF-2 has been uncovered utilizing the same cell surface receptor signaling cascade as MIF. Here we review MIF actions with respect to redox regulation in apoptosis and in tumor growth as well as its extracellular function with a focus on its potential role in brain diseases. We consider the possibility of MIF targeting in neurodegenerative processes and brain tumors by novel MIF-neutralizing approaches.
Insights
Macrophage migration inhibitory factor (MIF) is a key mediator in immunity and inflammation. Targeting MIF offers potential therapeutic strategies for brain diseases, including neurodegenerative conditions and brain tumors.
Area of Science:
- Biochemistry
- Immunology
- Oncology
Background:
- Macrophage migration inhibitory factor (MIF) is a pleiotropic cytokine with oxidoreductase and tautomerase activity.
- MIF is integral to innate and acquired immunity, the neuroendocrine axis, and pathogenesis of inflammation, cancer, and neoangiogenesis.
- MIF signaling is implicated in redox balance, apoptosis, senescence, and acts as a glucocorticoid antagonist, contributing to therapeutic resistance in brain tumors.
Purpose of the Study:
- To review the multifaceted roles of MIF, particularly its redox regulation in apoptosis and tumor growth.
- To explore the extracellular functions of MIF and its potential involvement in brain diseases.
- To consider novel MIF-neutralizing approaches for therapeutic intervention in neurodegenerative diseases and brain tumors.
Main Methods:
- Literature review of MIF's functions, signaling pathways, and therapeutic potential.
- Analysis of MIF's involvement in redox regulation, apoptosis, and tumor growth.
- Examination of MIF's extracellular roles and receptor-mediated pathways (CD74/CXCR2/CXCR4).
Main Results:
- MIF regulates essential cellular systems including redox balance, HIF-1, and p53-mediated apoptosis and senescence.
- MIF acts as an endogenous glucocorticoid antagonist, contributing to resistance in brain tumor therapies.
- A functional homolog, D-dopachrome tautomerase/MIF-2, utilizes the same cell surface receptor signaling cascade as MIF.
Conclusions:
- MIF is a relevant mediator in neurodegenerative and neurooncological diseases, though under-investigated.
- Targeting MIF presents a promising therapeutic avenue for brain diseases, including neuroprotection and anti-cancer strategies.
- Novel MIF-neutralizing approaches warrant further investigation for treating neurodegenerative processes and brain tumors.
