scholarly journals Cardiac macrophage migration inhibitory factor inhibits JNK pathway activation and injury during ischemia/reperfusion

2009 ◽  
Vol 119 (12) ◽  
pp. 3807-3816 ◽  
Author(s):  
Dake Qi ◽  
Xiaoyue Hu ◽  
Xiaohong Wu ◽  
Melanie Merk ◽  
Lin Leng ◽  
...  
Keyword(s):  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Ischemia Reperfusion ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Jnk Pathway ◽  
Pathway Activation

scholarly journals Inhibition of Macrophage Migration Inhibitory Factor Protects against Inflammation and Matrix Deposition in Kidney Tissues after Injury

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Hong Lu ◽  
Yongyu Bai ◽  
Lianfeng Wu ◽  
Weilong Hong ◽  
Yong Liang ◽  
...  
Keyword(s):  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Therapeutic Potential ◽  
Kidney Diseases ◽  
Ischemia Reperfusion ◽  
Specific Inhibitor ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Related Factors ◽  
Matrix Deposition

Background. Macrophage migration inhibitory factor (MIF) is an important immunoregulatory cytokine involved in inflammation, which may be one important reason resulting in matrix deposition in renal tissues after injury. However, the underlying mechanisms have not yet been elucidated.Methods and Results. We uncovered a crucial role of MIF in inflammation and collagen depositionin vivoandin vitro. In rats, ureteral obstruction induced tubular injury, matrix accumulation, and inflammatory cell infiltration. Additionally, enhanced MIF levels in the obstructed kidneys were closely related to the increasing numbers of CD68-positive macrophages. These obstruction-induced injuries can be relieved by recanalization, consequently resulting in downregulated expression of MIF and its receptor CD74. Similarly, ischemia reperfusion induced renal injury, and it was accompanied by elevated MIF levels and macrophages infiltration. In cultured tubular epithelial cells (TECs), aristolochic acid (AA) promoted matrix production and increased MIF expression, as well as the release of macrophage-related factors. Inhibition of MIF with an antagonist ISO-1 resulted in the abolishment of these genotypes in AA-treated TECs.Conclusion. MIF plays an important role in macrophage-related inflammation and matrix deposition in kidney tissues following injury. MIF as a specific inhibitor may have therapeutic potential for patients with inflammatory and fibrotic kidney diseases.

scholarly journals Macrophage Migration Inhibitory Factor as an Emerging Drug Target to Regulate Antioxidant Response Element System

2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Hiroshi Yukitake ◽  
Masayuki Takizawa ◽  
Haruhide Kimura
Keyword(s):  
Oxidative Stress ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Antioxidant Response ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Antioxidant Response Element ◽  
Response Element

Oxidative stress is involved in pathophysiology and pathological conditions of numerous human diseases. Thus, understanding the mechanisms underlying the redox homeostasis in cells and organs is valuable for discovery of therapeutic drugs for oxidative stress-related diseases. Recently, by applying chemical biology approach with an ARE activator, BTZO-1, we found macrophage migration inhibitory factor (MIF) as a new regulator of antioxidant response element- (ARE-) mediated gene transcription. BTZO-1 and its active derivatives bound to MIF and protected cells and organs from oxidative insults via ARE activation in animal models with oxidative stress such as ischemia/reperfusion injury, inflammatory bowel diseases, and septic shock. In this review, we briefly highlight key findings in understanding the MIF-ARE system.

scholarly journals Macrophage migration inhibitory factor (MIF) inhibitor 4-IPP downregulates stemness phenotype and mesenchymal trans-differentiation after irradiation in glioblastoma multiforme

PLoS ONE ◽  
2021 ◽  
Vol 16 (9) ◽  
pp. e0257375
Author(s):  
Shin Heon Lee ◽  
Hyung Joon Kwon ◽  
Saewhan Park ◽  
Chan Il Kim ◽  
Haseo Ryu ◽  
...  
Keyword(s):  
Radiation Therapy ◽  
Glioblastoma Multiforme ◽  
Signaling Pathway ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Dependent Manner ◽  
Dual Inhibitor ◽  
Pathway Activation

Radiation therapy is among the most essential treatment methods for glioblastoma multiforme (GBM). Radio-resistance and cancer stem cell properties can cause therapeutic resistance, cancer heterogeneity, and poor prognoses in association with GBM. Furthermore, the GBM subtype transition from proneural to the most malignant mesenchymal subtype after radiation therapy also accounts for high resistance to conventional treatments. Here, we demonstrate that the inhibition of macrophage migration inhibitory factor (MIF) and D-dopachrome tautomerase (DDT) by 4-iodo-6-phenylpyrimidine (4-IPP), a dual inhibitor targeting MIF and DDT, downregulates stemness phenotype, intracellular signaling cascades, mesenchymal trans-differentiation, and induces apoptosis in proneural glioma stem cells (GSCs). In an analysis of The Cancer Genome Atlas, high MIF and DDT expression were associated with poor prognosis. GSC growth was effectively inhibited by 4-IPP in a time- and dose-dependent manner, and 4-IPP combined with radiation therapy led to significantly reduced proliferation compared with radiation therapy alone. The expression of stemness factors, such as Olig2 and SOX2, and the expression of pAKT, indicating PI3K signaling pathway activation, were decreased in association with both 4-IPP monotherapy and combination treatment. The expression of mesenchymal markers, TGM2 and NF-κB, and expression of pERK (indicating MAPK signaling pathway activation) increased in association with radiation therapy alone but not with 4-IPP monotherapy and combination therapy. In addition, the combination of 4-IPP and radiation therapy significantly induced apoptosis compared to the monotherapy of 4-IPP or radiation. In vivo results demonstrated a significant tumor-suppressing effect of 4-IPP when combined with radiation therapy. Collectively, our results showed that the targeted inhibition of MIF and DDT has the potential to strengthen current clinical strategies by enhancing the anticancer effects of radiation therapy.

Macrophage Migration Inhibitory Factor Provides Cardioprotection During Ischemia/Reperfusion by Reducing Oxidative Stress

2011 ◽  
Vol 14 (7) ◽  
pp. 1191-1202 ◽  
Author(s):  
Kiyokazu Koga ◽  
Agnes Kenessey ◽  
Saul R. Powell ◽  
Cristina P. Sison ◽  
Edmund J. Miller ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Ischemia Reperfusion ◽  
Inhibitory Factor ◽  
Macrophage Migration

287: Macrophage Migration Inhibitory Factor and its Receptor CD74 are Upregulated in the Urothelium of Interstitial Cystitis Patients

2006 ◽  
Vol 175 (4S) ◽  
pp. 95-96 ◽  
Author(s):  
Pedro L. Vera ◽  
Kenneth A. lczkowski ◽  
Robert M. Moldwin ◽  
Leslie Kushner ◽  
Katherine L. Meyer-Siegler
Keyword(s):  
Interstitial Cystitis ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Macrophage Migration
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