scholarly journals Macrophage migration inhibitory factor has a permissive role in concanavalin A-induced cell death of human hepatoma cells through autophagy

2015 ◽  
Vol 6 (12) ◽  
pp. e2008-e2008 ◽  
Author(s):  
Y-C Lai ◽  
Y-C Chuang ◽  
C-P Chang ◽  
T-M Yeh
Keyword(s):  
Cell Death ◽  
Concanavalin A ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Hepatoma Cells ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Human Hepatoma ◽  
Human Hepatoma Cells ◽  
Permissive Role

Necrotic cell death increases the release of macrophage migration inhibitory factor by monocytes/macrophages

2020 ◽  
Vol 98 (9) ◽  
pp. 782-790 ◽  
Author(s):  
Wendy Dankers ◽  
Md Abul Hasnat ◽  
Vanesa Swann ◽  
Arwaf Alharbi ◽  
Jacinta PW Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Necrotic Cell Death ◽  
Macrophage Migration ◽  
Necrotic Cell

scholarly journals Macrophage Migration Inhibitory Factor Promotes Cell Death and Aggravates Neurologic Deficits after Experimental Stroke

2010 ◽  
Vol 31 (4) ◽  
pp. 1093-1106 ◽  
Author(s):  
Ana R Inácio ◽  
Karsten Ruscher ◽  
Lin Leng ◽  
Richard Bucala ◽  
Tomas Deierborg
Keyword(s):  
Cell Death ◽  
Migration Inhibitory Factor ◽  
Cortical Neurons ◽  
Macrophage Migration Inhibitory Factor ◽  
Acid Methyl Ester ◽  
Inhibitory Factor ◽  
Experimental Stroke ◽  
Macrophage Migration ◽  
Neurologic Deficits ◽  
The Brain

Multiple mechanisms contribute to tissue demise and functional recovery after stroke. We studied the involvement of macrophage migration inhibitory factor (MIF) in cell death and development of neurologic deficits after experimental stroke. Macrophage migration inhibitory factor is upregulated in the brain after cerebral ischemia, and disruption of the Mif gene in mice leads to a smaller infarct volume and better sensory-motor function after transient middle cerebral artery occlusion (tMCAo). In mice subjected to tMCAo, we found that MIF accumulates in neurons of the peri-infarct region, particularly in cortical parvalbumin-positive interneurons. Likewise, in cultured cortical neurons exposed to oxygen and glucose deprivation, MIF levels increase, and inhibition of MIF by (S,R)-3-(4-hydroxyphenyl)-4,5-dihydro-5-isoxazole acetic acid methyl ester (ISO-1) protects against cell death. Deletion of MIF in Mif−/− mice does not affect interleukin-1 β protein levels in the brain and serum after tMCAo. Furthermore, disruption of the Mif gene in mice does not affect CD68, but it is associated with higher galectin-3 immunoreactivity in the brain after tMCAo, suggesting that MIF affects the molecular/cellular composition of the macrophages/microglia response after experimental stroke. We conclude that MIF promotes neuronal death and aggravates neurologic deficits after experimental stroke, which implicates MIF in the pathogenesis of neuronal injury after stroke.

Lack of macrophage migration inhibitory factor protects mice against concanavalin A-induced liver injury

2006 ◽  
Vol 26 (3) ◽  
pp. 346-351 ◽  
Author(s):  
Hiroaki Nakajima ◽  
Hitoshi Takagi ◽  
Norio Horiguchi ◽  
Mitsuo Toyoda ◽  
Daisuke Kanda ◽  
...  
Keyword(s):  
Liver Injury ◽  
Concanavalin A ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Macrophage Migration

Novel inhibitors of macrophage migration inhibitory factor prevent cytokine-induced beta cell death

2014 ◽  
Vol 740 ◽  
pp. 683-689 ◽  
Author(s):  
Milica Vujicic ◽  
Ivana Nikolic ◽  
Tamara Krajnovic ◽  
Kai-Fan Cheng ◽  
Sonya VanPatten ◽  
...  
Keyword(s):  
Cell Death ◽  
Beta Cell ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Beta Cell Death
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