Редактирование: MIF

Macrophage migration inhibitory factor (EC 5.3.2.1) (MIF) (Glycosylation-inhibiting factor) (GIF) (L-dopachrome isomerase) (L-dopachrome tautomerase) (EC 5.3.3.12) (Phenylpyruvate tautomerase) [GLIF] [MMIF]

==Publications==

{{medline-entry
|title=Macrophage migration inhibitory factor rejuvenates aged human mesenchymal stem cells and improves myocardial repair.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31881006
|abstract=The beneficial functions of mesenchymal stem cells ([[MSC]]s) decline with age, limiting their therapeutic efficacy for myocardial infarction (MI). Macrophage migration inhibitory factor ([[MIF]]) promotes cell proliferation and survival. We investigated whether [[MIF]] overexpression could rejuvenate aged [[MSC]]s and increase their therapeutic efficacy in MI. Young and aged [[MSC]]s were isolated from the bone marrow of young and aged donors. Young [[MSC]]s, aged [[MSC]]s, and [[MIF]]-overexpressing aged [[MSC]]s were transplanted into the peri-infarct region in a rat MI model. Aged [[MSC]]s exhibited a lower proliferative capacity, lower [[MIF]] level, greater cell size, greater senescence-associated-β-galactosidase activity, and weaker paracrine effects than young [[MSC]]s. Knocking down [[MIF]] in young [[MSC]]s induced cellular senescence, whereas overexpressing [[MIF]] in aged [[MSC]]s reduced cellular senescence. [[MIF]] rejuvenated aged [[MSC]]s by activating autophagy, an effect largely reversed by the autophagy inhibitor 3-methyladenine. [[MIF]]-overexpressing aged [[MSC]]s induced angiogenesis and prevented cardiomyocyte apoptosis to a greater extent than aged [[MSC]]s, and had improved heart function and cell survival more effectively than aged [[MSC]]s four weeks after MI. Thus, [[MIF]] rejuvenated aged [[MSC]]s by activating autophagy and enhanced their therapeutic efficacy in MI, suggesting a novel [[MSC]]-based therapeutic strategy for cardiovascular diseases in the aged population.
|mesh-terms=* Adolescent
* Aged
* Aged, 80 and over
* Aging
* Animals
* Animals, Newborn
* Cellular Senescence
* Humans
* Macrophage Migration-Inhibitory Factors
* Mesenchymal Stem Cell Transplantation
* Mesenchymal Stem Cells
* Myocardial Infarction
* Myocardium
* Myocytes, Cardiac
* Rats
* Rats, Sprague-Dawley
* Young Adult
|keywords=* macrophage migration inhibitory factor
* mesenchymal stem cells
* myocardial infarction
* rejuvenation
* senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6949107
}}
{{medline-entry
|title=Mitochondrial DNA alterations in aged macrophage migration inhibitory factor-knockout mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31381889
|abstract=The age-induced, exponential accumulation of mitochondrial DNA (mtDNA) deletion mutations contributes to muscle fiber loss. The causes of these mutations are not known. Systemic inflammation is associated with decreased muscle mass in older adults and is implicated in the formation of sporadic mtDNA deletions. Macrophage migration inhibitory factor knockout ([[MIF]]-KO) mice are long-lived with decreased inflammation. We hypothesized that aged [[MIF]]-KO mice would have lower mtDNA deletion frequencies and fewer electron transport chain (ETC) deficient fibers. We measured mtDNA copy number and mutation frequency as well as the number and length of ETC deficient fibers in 22-month old [[MIF]]-KO and [[F2]] hybrid control mice. We also measured mtDNA copy number and deletion frequency in female UM-HET3 mice, a strain whose lifespan matches the [[MIF]]-KO mice. We did not observe a significant effect of [[MIF]] ablation on muscle mtDNA deletion frequency. There was a significantly lower mtDNA copy number in the [[MIF]]-KO mice and the lifespan-matched UM-HET3 mice compared to the [[F2]] hybrids, suggesting the importance of genetic background in mtDNA copy number control. Our data do not support a definitive role for [[MIF]] in age-induced mtDNA deletions.
|mesh-terms=* Animals
* Cellular Senescence
* DNA Copy Number Variations
* DNA, Mitochondrial
* Intramolecular Oxidoreductases
* Longevity
* Macrophage Migration-Inhibitory Factors
* Macrophages
* Mice
* Mice, Knockout
|keywords=* Macrophage migration inhibitory factor
* Mitochondrial DNA
* Mutation
* Skeletal muscle
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6718337
}}
{{medline-entry
|title=Macrophage migration inhibitory factor knockdown inhibit viability and induce apoptosis of PVM/Ms.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/28990052
|abstract=Previous studies have suggested that macrophage migration inhibitory factor ([[MIF]]) serves an important role in hearing function; however, the underlying mechanism remains unclear. In the present study, perivascular‑resident macrophage‑like melanocytes (PVM/Ms) from the stria vascularis of the lateral cochlear wall in young and aged mice were isolated. The mRNA and protein expression levels of [[MIF]] were determined using reverse transcription‑quantitative polymerase chain reaction analysis, and western blotting, respectively. [[MIF]] expression was knocked down in vitro and in vivo using small interfering RNA. Cell viability was determined using an MTT assay and cell apoptosis was determined using flow cytometry analysis. The hearing ability was assessed through the auditory brain stem response in vivo. The results of the current study demonstrated that the expression of [[MIF]] was significantly downregulated in aged mice compared with in young mice. Furthermore, the viability of PVM/Ms in aged mice was significantly decreased and the number of apoptotic PVM/Ms was significantly increased compared with that in young mice. Further studies demonstrated that the [[MIF]] knockdown accentuated hearing loss in young mice as compared with the scramble control group. In addition, the [[MIF]] knockdown in PVM/Ms significantly inhibited cell viability and lead to a significant increase in the apoptotic cell number as compared with the control group. In summary, these results revealed that the [[MIF]] knockdown significantly accentuates hearing loss in young mice in vivo, and significantly inhibits the viability and induces the apoptosis of PVM/Ms in vitro. Thus, the results of the present study may provide a novel potential therapeutic approach and prevention method for presbycusis.
|mesh-terms=* Aging
* Animals
* Apoptosis
* Cell Count
* Cell Survival
* Cochlea
* Down-Regulation
* Gene Knockdown Techniques
* Hearing Loss
* Macrophage Migration-Inhibitory Factors
* Macrophages
* Melanocytes
* Mice, Inbred C57BL

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5779918
}}
{{medline-entry
|title=Endogenous macrophage migration inhibitory factor reduces the accumulation and toxicity of misfolded [[SOD1]] in a mouse model of ALS.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27551074
|abstract=Mutations in superoxide dismutase ([[SOD1]]) cause amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disease characterized by the loss of upper and lower motor neurons in the brain and spinal cord. It has been suggested that the toxicity of mutant [[SOD1]] results from its misfolding and accumulation on the cytoplasmic faces of intracellular organelles, including the mitochondria and endoplasmic reticulum (ER) of ALS-affected tissues. Recently, macrophage migration inhibitory factor ([[MIF]]) was shown to directly inhibit the accumulation of misfolded [[SOD1]] and its binding to intracellular membranes, but the role of endogenous [[MIF]] in modulating [[SOD1]] misfolding in vivo remains unknown. To elucidate this role, we bred [[MIF]]-deficient mice with [[SOD1]](G85R) mice, which express a dismutase-inactive mutant of [[SOD1]] and are considered a model of familial ALS. We found that the accumulation of misfolded [[SOD1]], its association with mitochondrial and ER membranes, and the levels of sedimentable insoluble [[SOD1]] aggregates were significantly higher in the spinal cords of [[SOD1]](G85R)-[[MIF]](-/-) mice than in their [[SOD1]](G85R)-[[MIF]]( / ) littermates. Moreover, increasing [[MIF]] expression in neuronal cultures inhibited the accumulation of misfolded [[SOD1]] and rescued from mutant [[SOD1]]-induced cell death. In contrast, the complete elimination of endogenous [[MIF]] accelerated disease onset and late disease progression and shortened the lifespan of the [[SOD1]](G85R) mutant mice. These findings indicate that [[MIF]] plays a significant role in the folding and misfolding of [[SOD1]] in vivo, and they have implications for the potential therapeutic role of up-regulating [[MIF]] within the nervous system to modulate the selective accumulation of misfolded [[SOD1]].
|mesh-terms=* Amyotrophic Lateral Sclerosis
* Animals
* Cell Death
* Disease Models, Animal
* Endoplasmic Reticulum
* Female
* Gene Expression
* Humans
* Intramolecular Oxidoreductases
* Longevity
* Macrophage Migration-Inhibitory Factors
* Male
* Mice
* Mice, Knockout
* Mitochondria
* Mutation
* Neurons
* Primary Cell Culture
* Protein Aggregates
* Protein Folding
* Spinal Cord
* Superoxide Dismutase-1
|keywords=* ALS
* MIF
* misfolded SOD1
* mutant SOD1
* mutant SOD1 mouse
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5018779
}}
{{medline-entry
|title=Macrophage Migration Inhibitory Factor ([[MIF]]) Deficiency Exacerbates Aging-Induced Cardiac Remodeling and Dysfunction Despite Improved Inflammation: Role of Autophagy Regulation.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26940544
|abstract=Aging leads to unfavorable geometric and functional sequelae in the heart. The proinflammatory cytokine macrophage migration inhibitory factor ([[MIF]]) plays a role in the maintenance of cardiac homeostasis under stress conditions although its impact in cardiac aging remains elusive. This study was designed to evaluate the role of [[MIF]] in aging-induced cardiac anomalies and the underlying mechanism involved. Cardiac geometry, contractile and intracellular Ca(2 ) properties were examined in young (3-4 mo) or old (24 mo) wild type and [[MIF]] knockout ([[MIF]](-/-)) mice. Our data revealed that [[MIF]] knockout exacerbated aging-induced unfavorable structural and functional changes in the heart. The detrimental effect of [[MIF]] knockout was associated with accentuated loss in cardiac autophagy with aging. Aging promoted cardiac inflammation, the effect was attenuated by [[MIF]] knockout. Intriguingly, aging-induced unfavorable responses were reversed by treatment with the autophagy inducer rapamycin, with improved myocardial ATP availability in aged WT and [[MIF]](-/-) mice. Using an in vitro model of senescence, [[MIF]] knockdown exacerbated doxorubicin-induced premature senescence in H9C2 myoblasts, the effect was ablated by [[MIF]] replenishment. Our data indicated that [[MIF]] knockout exacerbates aging-induced cardiac remodeling and functional anomalies despite improved inflammation, probably through attenuating loss of autophagy and ATP availability in the heart.
|mesh-terms=* Adenosine Triphosphate
* Aging
* Animals
* Autophagy
* Cell Line
* Cellular Senescence
* Heart
* Inflammation
* Intramolecular Oxidoreductases
* Macrophage Migration-Inhibitory Factors
* Macrophages
* Male
* Mice
* Mice, Inbred C57BL
* Mice, Knockout
* Myocardium
* Sirolimus
* Ventricular Remodeling

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4778027
}}
{{medline-entry
|title=Age-dependent alterations in the inflammatory response to pulmonary challenge.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26318747
|abstract=The aging lung is increasingly susceptible to infectious disease. Changes in pulmonary physiology and function are common in older populations, and in those older than 60 years, pneumonia is the major cause of infectious death. Understanding age-related changes in the innate and adaptive immune systems, and how they affect both pulmonary and systemic responses to pulmonary challenge are critical to the development of novel therapeutic strategies for the treatment of the elderly patient. In this observational study, we examined age-associated differences in inflammatory responses to pulmonary challenge with cell wall components from Gram-positive bacteria. Thus, male Sprague-Dawley rats, aged 6 months or greater than 18 months (approximating humans of 20 and 55-65 years), were challenged, intratracheally, with lipoteichoic acid and peptidoglycan. Cellular and cytokine evaluations were performed on both bronchoalveolar lavage fluid (BAL) and plasma, 24 h post-challenge. The plasma concentration of free thyroxine, a marker of severity in non-thyroidal illness, was also evaluated. The older animals had an increased chemotactic gradient in favor of the airspaces, which was associated with a greater accumulation of neutrophils and protein. Furthermore, macrophage migration inhibitory factor ([[MIF]]), an inflammatory mediator and putative biomarker in acute lung injury, was increased in both the plasma and BAL of the older, but not young animals. Conversely, plasma free thyroxine, a natural inhibitor of [[MIF]], was decreased in the older animals. These findings identify age-associated inflammatory/metabolic changes following pulmonary challenge that it may be possible to manipulate to improve outcome in the older, critically ill patient.
|mesh-terms=* Adult
* Age Factors
* Aged
* Animals
* Chemotaxis
* Humans
* Lipopolysaccharides
* Macrophage Migration-Inhibitory Factors
* Male
* Middle Aged
* Neutrophils
* Peptidoglycan
* Pneumonia
* Rats
* Rats, Sprague-Dawley
* Teichoic Acids
* Thyroxine
* Young Adult
|keywords=* Acute lung injury
* Aging
* Pneumonia
* Thyroxine
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4648978
}}
{{medline-entry
|title=Role of macrophage migration inhibitory factor in age-related lung disease.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/25957294
|abstract=The prevalence of many common respiratory disorders, including pneumonia, chronic obstructive lung disease, pulmonary fibrosis, and lung cancer, increases with age. Little is known of the host factors that may predispose individuals to such diseases. Macrophage migration inhibitory factor ([[MIF]]) is a potent upstream regulator of the immune system. [[MIF]] is encoded by variant alleles that occur commonly in the population. In addition to its role as a proinflammatory cytokine, a growing body of literature demonstrates that [[MIF]] influences diverse molecular processes important for the maintenance of cellular homeostasis and may influence the incidence or clinical manifestations of a variety of chronic lung diseases. This review highlights the biological properties of [[MIF]] and its implication in age-related lung disease. 
|mesh-terms=* Aging
* Animals
* Cytokines
* Humans
* Inflammation
* Intramolecular Oxidoreductases
* Lung Neoplasms
* Macrophage Migration-Inhibitory Factors
* Mice
* Pneumonia, Bacterial
* Pulmonary Disease, Chronic Obstructive
|keywords=* MIF
* innate immunity
* lung
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4491511
}}
{{medline-entry
|title=Macrophage migration inhibitory factor confers resistance to senescence through [[CD74]]-dependent AMPK-FOXO3a signaling in mesenchymal stem cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/25896286
|abstract=Mesenchymal stem cells (MSCs)-based therapies have had positive outcomes in animal models of cardiovascular diseases. However, the number and function of MSCs decline with age, reducing their ability to contribute to endogenous injury repair. The potential of stem cells to restore damaged tissue in older individuals can be improved by specific pretreatment aimed at delaying senescence and improving their regenerative properties. Macrophage migration inhibitory factor ([[MIF]]) is a proinflammatory cytokine that modulates age-related signaling pathways, and hence is a good candidate for rejuvenative function. Bone marrow-derived mesenchymal stem cells (BM-MSCs) were isolated from young (6-month-old) or aged (24-month-old) male donor rats. Cell proliferation was measured using the CCK8 cell proliferation assay; secretion of VEGF, bFGF, [[HGF]], and IGF was assessed by RT-qPCR and ELISA. Apoptosis was induced by hypoxia and serum deprivation (hypoxia/SD) for up to 6 hr, and examined by flow cytometry. Expression levels of AMP-activated protein kinase (AMPK) and forkhead box class O 3a (FOXO3a) were detected by Western blotting. [[CD74]] expression was assayed using RT-qPCR, Western blotting, and immunofluorescence. In this study, we found that MSCs isolated from the bone marrow of aged rats displayed reduced proliferative capacity, impaired ability to mediate paracrine signaling, and lower resistance to hypoxia/serum deprivation-induced apoptosis, when compared to younger MSCs. Interestingly, pretreatment of aged MSCs with [[MIF]] enhanced their growth, paracrine function and survival. We detected enhanced secretion of VEGF, bFGF, [[HGF]], and IGF from [[MIF]]-treated MSCs using ELISA. Finally, we show that hypoxia/serum deprivation-induced apoptosis is inhibited in aged MSCs following [[MIF]] exposure. Next, we found that the mechanism underlying the rejuvenating function of [[MIF]] involves increased [[CD74]]-dependent phosphorylation of AMPK and FOXO3a. Furthermore, this effect was abolished when [[CD74]], AMPK, or FOXO3a expression was silenced using small-interfering RNAs(siRNA). [[MIF]] can rejuvenate MSCs from a state of age-induced senescence by interacting with [[CD74]] and subsequently activating AMPK-FOXO3a signaling pathways. Pretreatment of MSCs with [[MIF]] may have important therapeutic implications in restoration or rejuvenation of endogenous bone marrow-MSCs in aged individuals.
|mesh-terms=* AMP-Activated Protein Kinases
* Aging
* Animals
* Antigens, Differentiation, B-Lymphocyte
* Apoptosis
* Bone Marrow Cells
* Cell Hypoxia
* Cell Proliferation
* Cells, Cultured
* Down-Regulation
* Forkhead Box Protein O3
* Forkhead Transcription Factors
* Histocompatibility Antigens Class II
* Intercellular Signaling Peptides and Proteins
* Intramolecular Oxidoreductases
* Macrophage Migration-Inhibitory Factors
* Male
* Mesenchymal Stem Cells
* Myocardium
* Paracrine Communication
* Phosphorylation
* RNA Interference
* Rats
* Rats, Sprague-Dawley
* Signal Transduction

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4453287
}}
{{medline-entry
|title=Role of macrophage migration inhibitory factor in age-related hearing loss.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/25194790
|abstract=Hearing loss related to aging is the most common sensory disorder among elderly individuals. Macrophage migration inhibitory factor ([[MIF]]) is a multi-functional molecule. The aim of this study was to identify the role of [[MIF]] in the inner ear. [[MIF]]-deficient mice ([[MIF]](-/-) mice) of BALB/c background and wild-type BALB/c mice were used in this study. Expression of [[MIF]] protein in the inner ear was examined by immunohistochemistry in wild-type mice (WT). The hearing function was assessed by the click-evoked auditory brainstem response in both [[MIF]](-/-) mice and WT at 1, 3, 6, 9, 12, and 18months of age. Morphological examination of the cochlea was also performed using scanning electron microscopy and light microscopy. [[MIF]] was observed in the spiral ligament, stria vascularis, Reissner's membrane, spiral ganglion cells (SGCs), saccular macula, and membranous labyrinth. The [[MIF]](-/-) mice had a significant hearing loss as compared with the WT at 9, 12, and 18months of age. In the [[MIF]](-/-) mice, scanning electron microscopy showed that the outer cochlear hair cells were affected, but that the inner cochlear hair cells were relatively well preserved. The number of SGCs was lower in the [[MIF]](-/-) mice. [[MIF]] was strongly expressed in the mouse inner ear. Older [[MIF]](-/-) mice showed accelerated age-related hearing loss and morphological inner ear abnormalities. These findings suggest that [[MIF]] plays an important role in the inner ear of mice. 
|mesh-terms=* Aging
* Animals
* Auditory Threshold
* Ear, Inner
* Evoked Potentials, Auditory, Brain Stem
* Hearing Loss
* Immunohistochemistry
* Intramolecular Oxidoreductases
* Macrophage Migration-Inhibitory Factors
* Mice, Inbred BALB C
* Mice, Knockout
* Microscopy, Electron, Scanning
|keywords=* cochlea
* ear
* hair cell
* hearing loss
* macrophage migration inhibitory factor
* spiral ganglion cells
|full-text-url=https://sci-hub.do/10.1016/j.neuroscience.2014.08.042
}}
{{medline-entry
|title=Macrophage migration inhibitory factor deficiency in chronic obstructive pulmonary disease.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/24441872
|abstract=The pathogenesis of chronic obstructive pulmonary disease (COPD) remains poorly understood. Cellular senescence and apoptosis contribute to the development of COPD; however, crucial regulators of these underlying mechanisms remain unknown. Macrophage migration inhibitory factor ([[MIF]]) is a pleiotropic cytokine that antagonizes both apoptosis and premature senescence and may be important in the pathogenesis of COPD. This study examines the role of [[MIF]] in the pathogenesis of COPD. Mice deficient in [[MIF]] (Mif(-/-)) or the [[MIF]] receptor [[CD74]] (Cd74(-/-)) and wild-type (WT) controls were aged for 6 mo. Both Mif(-/-) and Cd74(-/-) mice developed spontaneous emphysema by 6 mo of age compared with WT mice as measured by lung volume and chord length. This was associated with activation of the senescent pathway markers p53/21 and p16. Following exposure to cigarette smoke, Mif(-/-) mice were more susceptible to the development of COPD and apoptosis compared with WT mice. [[MIF]] plasma concentrations were measured in a cohort of 224 human participants. Within a subgroup of older current and former smokers (n = 72), [[MIF]] concentrations were significantly lower in those with COPD [8.8, 95%CI (6.7-11.0)] compared with those who did not exhibit COPD [12.7 ng/ml, 95%CI (10.6-14.8)]. Our results suggest that both [[MIF]] and the [[MIF]] receptor [[CD74]] are required for maintenance of normal alveolar structure in mice and that decreases in [[MIF]] are associated with COPD in human subjects. 
|mesh-terms=* Adolescent
* Adult
* Age Factors
* Aged
* Aged, 80 and over
* Animals
* Apoptosis
* Cellular Senescence
* Cyclin-Dependent Kinase Inhibitor p16
* Cyclin-Dependent Kinase Inhibitor p21
* Emphysema
* Female
* Humans
* Intramolecular Oxidoreductases
* Lung
* Macrophage Migration-Inhibitory Factors
* Male
* Mice
* Mice, Inbred C57BL
* Mice, Knockout
* Middle Aged
* Pulmonary Disease, Chronic Obstructive
* Receptors, Immunologic
* Smoke
* Smoking
* Tobacco
* Tumor Suppressor Protein p53
* Young Adult
|keywords=* CD74
* COPD
* MIF
* apoptosis
* emphysema
* senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3949087
}}
{{medline-entry
|title=Strength training and testosterone treatment have opposing effects on migration inhibitor factor levels in ageing men.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/24089589
|abstract=The beneficial effects of testosterone treatment (TT) are debated. Double-blinded, placebo-controlled study of six months TT (gel) in 54 men aged 60-78 with bioavailable testosterone (BioT) <7.3 nmol/L and waist >94 cm randomized to TT (50-100 mg/day, n = 20), placebo (n = 18), or strength training (ST) (n = 16) for 24 weeks. Moreover, the ST group was randomized to TT (n = 7) or placebo (n = 9) after 12 weeks. Chemokines ([[MIF]], MCP-1, and [[MIP]]-1 α ) and lean body mass (LBM), total, central, extremity, visceral, and subcutaneous (SAT) fat mass established by DXA and MRI. Results. From 0 to 24 weeks, [[MIF]] and SAT decreased during ST   placebo versus placebo, whereas BioT and LBM were unchanged. TT decreased fat mass (total, central, extremity, and SAT) and increased BioT and LBM versus placebo. [[MIF]] levels increased during TT versus ST   placebo. ST   TT decreased fat mass (total, central, and extremity) and increased BioT and LBM versus placebo. From 12 to 24 weeks, MCP-1 levels increased during TT versus placebo and MCP-1 levels decreased during ST   placebo versus placebo. ST   placebo was associated with decreased [[MIF]] levels suggesting decreased inflammatory activity. TT may be associated with increased inflammatory activity.
|mesh-terms=* Absorptiometry, Photon
* Aged
* Aging
* Body Composition
* Chemokine CCL2
* Chemokine CCL3
* Chemokines
* Double-Blind Method
* Gels
* Humans
* Inflammation
* Intramolecular Oxidoreductases
* Macrophage Migration-Inhibitory Factors
* Magnetic Resonance Imaging
* Male
* Middle Aged
* Resistance Training
* Testosterone
* Time Factors
* Treatment Outcome

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3781991
}}
{{medline-entry
|title=Role of migratory inhibition factor in age-related susceptibility to radiation lung injury via NF-E2-related factor-2 and antioxidant regulation.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/23526214
|abstract=Microvascular injury and increased vascular leakage are prominent features of radiation-induced lung injury (RILI), and often follow cancer-associated thoracic irradiation. Our previous studies demonstrated that polymorphisms in the gene ([[MIF]]) encoding macrophage migratory inhibition factor ([[MIF]]), a multifunctional pleiotropic cytokine, confer susceptibility to acute inflammatory lung injury and increased vascular permeability, particularly in senescent mice. In this study, we exposed wild-type and genetically engineered mif(-/-) mice to 20 Gy single-fraction thoracic radiation to investigate the age-related role of [[MIF]] in murine RILI (mice were aged 8 wk, 8 mo, or 16 mo). Relative to 8-week-old mice, decreased [[MIF]] was observed in bronchoalveolar lavage fluid and lung tissue of 8- to 16-month-old wild-type mice. In addition, radiated 8- to 16-month-old mif(-/-) mice exhibited significantly decreased bronchoalveolar lavage fluid total antioxidant concentrations with progressive age-related decreases in the nuclear expression of NF-E2-related factor-2 (Nrf2), a transcription factor involved in antioxidant gene up-regulation in response to reactive oxygen species. This was accompanied by decreases in both protein concentrations (NQO1, [[GCLC]], and heme oxygenase-1) and mRNA concentrations (Gpx1, Prdx1, and Txn1) of Nrf2-influenced antioxidant gene targets. In addition, [[MIF]]-silenced (short, interfering RNA) human lung endothelial cells failed to express Nrf2 after oxidative (H2O2) challenge, an effect reversed by recombinant [[MIF]] administration. However, treatment with an antioxidant (glutathione reduced ester), but not an Nrf2 substrate (N-acetyl cysteine), protected aged mif(-/-) mice from RILI. These findings implicate an important role for [[MIF]] in radiation-induced changes in lung-cell antioxidant concentrations via Nrf2, and suggest that [[MIF]] may contribute to age-related susceptibility to thoracic radiation. 
|mesh-terms=* Acute Lung Injury
* Aging
* Animals
* Bronchoalveolar Lavage Fluid
* Cells, Cultured
* Gamma Rays
* Heme Oxygenase-1
* Humans
* Hydrogen Peroxide
* Intramolecular Oxidoreductases
* Macrophage Migration-Inhibitory Factors
* Membrane Proteins
* Mice
* Mice, Knockout
* NAD(P)H Dehydrogenase (Quinone)
* NF-E2-Related Factor 2
* Oxidants
* Radiation Injuries, Experimental

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3824032
}}