A functional role of Macrophage Migration Inhibitory Factor (MIF) for liver steatosis in mice by activation of AMP kinase

2012 ◽  
Vol 50 (01) ◽  
Author(s):  
D Heinrichs ◽  
M Knauel ◽  
A Nellen ◽  
P Schmitz ◽  
C Trautwein ◽  
...  
2011 ◽  
Vol 3 (3) ◽  
pp. 135-142
Author(s):  
Warren B. Nothnick ◽  
Arlene Colvin ◽  
Kai Fan Cheng ◽  
Yousef Al-Abed

Aim Macrophage migration inhibitory factor (MIF) is a cytokine whose expression is elevated in endometriotic tissue from women with the disease but the functional role of this factor in the pathogenesis of the disease is uncertain. The objective of the current study was to examine the role of MIF in the pathogenesis of endometriosis. Method Experimental endometriosis was induced in mice and the ability of the MIF antagonist, ISO-1, to reduce endometriotic implant size was assessed. Results Administration of ISO-1 resulted in a significant reduction in implant size and vascularity (as assessed by Flk1 mRNA expression) which was not associated with an alteration in the reproductive cycle. Conclusion These data suggest that inhibition of MIF activity is associated with a significant reduction in endometriotic implant size and leads us to speculate that a similar approach of targeting MIF may prove useful in treating endometriosis in humans.


2012 ◽  
Vol 189 (8) ◽  
pp. 3905-3913 ◽  
Author(s):  
Susanna Choi ◽  
Hang-Rae Kim ◽  
Lin Leng ◽  
Insoo Kang ◽  
William L. Jorgensen ◽  
...  

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
XiYong Yu ◽  
ZhiXin Shan ◽  
QiuXiong Lin ◽  
ShiXia Cai ◽  
Min Yang ◽  
...  

2002 ◽  
Vol 283 (1) ◽  
pp. L156-L162 ◽  
Author(s):  
Yoshinori Tanino ◽  
Hironi Makita ◽  
Kenji Miyamoto ◽  
Tomoko Betsuyaku ◽  
Yoshinori Ohtsuka ◽  
...  

Macrophage migration inhibitory factor (MIF) is a unique cytokine that reportedly overrides the anti-inflammatory effect of endogenous glucocorticoids. MIF has been demonstrated to be involved in a variety of inflammatory diseases. In this study, we examined the role of MIF in bleomycin (BLM)-induced lung injury and fibrosis. The levels of MIF in lung tissues and bronchoalveolar lavage fluids were significantly increased in the period 5–10 days after intratracheal administration of BLM. Treatment with the anti-MIF antibody significantly reduced the mortality at 14 days and the histopathological lung injury score at 10 days. These effects were accompanied with significant suppression of the accumulation of inflammatory cells in the alveolar space and tumor necrosis factor-α in the lungs at 7 days. However, the anti-MIF antibody did not affect either the content of lung hydroxyproline or the histopathological lung fibrosis score at 21 days after BLM. These data provide further evidence for the crucial role of MIF in acute lung inflammation but do not support the involvement of MIF in lung fibrosis induced by BLM in mice.


2018 ◽  
Vol 2018 (2) ◽  
Author(s):  
Mohamed Ahmed ◽  
Edmund Miller

Macrophage migration inhibitory factor (MIF) has been described as a pro-inflammatory cytokine and regulator of neuro-endocrine function. It plays an important upstream role in the inflammatory cascade by promoting the release of other inflammatory cytokines such as TNF-alpha and IL-6, ultimately triggering a chronic inflammatory immune response. As lungs can synthesize and release MIF, many studies have investigated the potential role of MIF as a biomarker in assessment of patients with pulmonary arterial hypertension (PAH) and using anti-MIFs as a new therapeutic modality for PAH.


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