Macrophage migration inhibitory factor (MIF) promotes cell survival and proliferation of neural stem/progenitor cells

Development ◽  
2012 ◽  
Vol 139 (19) ◽  
pp. e1908-e1908
Author(s):  
S. Ohta ◽  
A. Misawa ◽  
R. Fukaya ◽  
S. Inoue ◽  
Y. Kanemura ◽  
...  
Keyword(s):  
Cell Survival ◽  
Progenitor Cells ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Neural Stem Progenitor Cells ◽  
Cell Survival And Proliferation

Macrophage migration inhibitory factor (MIF) promotes cell survival and proliferation of neural stem/progenitor cells

2020 ◽  
Author(s):  
Lungwani Muungo
Keyword(s):  
Cell Survival ◽  
Progenitor Cells ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Ganglionic Eminence ◽  
Neural Stem Progenitor Cells

In a previous study, we showed that murine dendritic cells (DCs) can increase the number of neural stem/progenitor cells (NSPCs) in vitroand in vivo. In the present study, we identified macrophage migration inhibitory factor (MIF) as a novel factor that can support theproliferation and/or survival of NSPCs in vitro. MIF is secreted by DCs and NSPCs, and its function in the normal brain remains largelyunknown. It was previously shown that in macrophages, MIF binds to a CD74–CD44 complex. In the present study, we observed theexpression of MIF receptors in mouse ganglionic-eminence-derived neurospheres using flow cytometry in vitro. We also found CD74expression in the ganglionic eminence of E14 mouse brains, suggesting that MIF plays a physiological role in vivo. MIF increased thenumber of primary and secondary neurospheres. By contrast, retrovirally expressed MIF shRNA and MIF inhibitor (ISO-1) suppressedprimary and secondary neurosphere formation, as well as cell proliferation. In the neurospheres, MIF knockdown by shRNA increasedcaspase 3/7 activity, and MIF increased the phosphorylation of Akt, Erk, AMPK and Stat3 (Ser727), as well as expression of Hes3 and Egfr,the products of which are known to support cell survival, proliferation and/or maintenance of NSPCs. MIF also acted as a chemoattractantfor NSPCs. These results show that MIF can induce NSPC proliferation and maintenance by multiple signaling pathways actingsynergistically, and it may be a potential therapeutic factor, capable of activating NSPC, for the treatment of degenerative brain disorders.

scholarly journals Macrophage Migration Inhibitory Factor Induces B Cell Survival by Activation of a CD74-CD44 Receptor Complex

2007 ◽  
Vol 283 (5) ◽  
pp. 2784-2792 ◽  
Author(s):  
Yael Gore ◽  
Diana Starlets ◽  
Nitsan Maharshak ◽  
Shirly Becker-Herman ◽  
Utako Kaneyuki ◽  
...  
Keyword(s):  
B Cell ◽  
Cell Survival ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Receptor Complex ◽  
Cd44 Receptor ◽  
B Cell Survival

scholarly journals CD74 is a novel transcription regulator

2016 ◽  
Vol 114 (3) ◽  
pp. 562-567 ◽  
Author(s):  
Naama Gil-Yarom ◽  
Lihi Radomir ◽  
Lital Sever ◽  
Matthias P. Kramer ◽  
Hadas Lewinsky ◽  
...  
Keyword(s):  
Cell Survival ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Cell Surface Receptor ◽  
Macrophage Migration ◽  
Regulation Of Expression ◽  
Surface Receptor ◽  
Related Transcription Factor ◽  
A Cell

CD74 is a cell-surface receptor for the cytokine macrophage migration inhibitory factor. Macrophage migration inhibitory factor binding to CD74 induces its intramembrane cleavage and the release of its cytosolic intracellular domain (CD74–ICD), which regulates cell survival. In the present study, we characterized the transcriptional activity of CD74–ICD in chronic lymphocytic B cells. We show that following CD74 activation, CD74–ICD interacts with the transcription factors RUNX (Runt related transcription factor) and NF-κB and binds to proximal and distal regulatory sites enriched for genes involved in apoptosis, immune response, and cell migration. This process leads to regulation of expression of these genes. Our results suggest that identifying targets of CD74 will help in understanding of essential pathways regulating B-cell survival in health and disease.

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