Macrophage migration inhibitory factor provides cardioprotection during ischemia/reperfusion by reducing oxidative stress

Macrophage migration inhibitory factor provides cardioprotection during ischemia/reperfusion by reducing oxidative stress

Macrophage migration inhibitory factor (MIF) is a multifunctional protein that exhibits an intrinsic thiol protein oxidoreductase activity and proinflammatory activities. In the present study to examine intracellular MIF redox function, exposure of MIF-deficient cardiac fibroblasts to oxidizing cond...

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Veröffentlicht in:Antioxidants & redox signaling 2011-04, Vol.14 (7), p.1191-1202
Hauptverfasser: Koga, Kiyokazu, Kenessey, Agnes, Powell, Saul R, Sison, Cristina P, Miller, Edmund J, Ojamaa, Kaie
Format: Artikel
Sprache:eng
Schlagworte:
Aconitate Hydratase - metabolism
Animals
Catalase - chemistry
Cell Survival
Cells, Cultured
Cytochromes c - metabolism
Fibroblasts - metabolism
Glutathione - metabolism
Glutathione Disulfide - metabolism
Glutathione Peroxidase - metabolism
Glutathione Reductase - metabolism
Heart Ventricles - pathology
Heart Ventricles - physiopathology
Hemodynamics
Homeodomain Proteins - metabolism
Hydrogen Peroxide - pharmacology
Intramolecular Oxidoreductases - deficiency
Intramolecular Oxidoreductases - genetics
Intramolecular Oxidoreductases - metabolism
Ischemia
Macrophage Migration-Inhibitory Factors - deficiency
Macrophage Migration-Inhibitory Factors - genetics
Macrophage Migration-Inhibitory Factors - metabolism
Macrophages
Mice
Mice, Inbred C57BL
Mice, Knockout
Mitochondria, Heart - metabolism
Myocardial Reperfusion Injury - metabolism
Myocardial Reperfusion Injury - pathology
Myocardium - metabolism
Myocardium - pathology
Oxidation-Reduction
Oxidative Stress
Physiological aspects
Prevention
Reactive Oxygen Species - metabolism
Superoxide Dismutase - metabolism
Thioredoxins - metabolism
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Zusammenfassung:Macrophage migration inhibitory factor (MIF) is a multifunctional protein that exhibits an intrinsic thiol protein oxidoreductase activity and proinflammatory activities. In the present study to examine intracellular MIF redox function, exposure of MIF-deficient cardiac fibroblasts to oxidizing conditions resulted in a 2.3-fold increase (p 
ISSN:1523-0864
1557-7716
DOI:10.1089/ars.2010.3163