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PubMed1976

MIF, TRH, and simian social and motor behavior.

MSH-release-inhibiting factor (MIF) and thyrotropin-releasing hormone (TRH) both have been reported to modify mood and activity in man. These two hypothalamic peptides were given intramuscularly across a 1000-fold dose range to 5 juvenile male M. nemestrina monkeys living in a social group. Motor activity was recorded automatically, and an observer counted various social behaviors. MIF increased motor activity for up to 11 hr. It decreased quiet foraging behavior, but did not change behaviors of social interaction. TRH did not stimulate motor behavior; high doses strongly suppressed it and produced apparent somatic distress. TRH increased behaviors of quiet rest and association and decreased environment exploration and low-intensity dominance behaviors. The lowest dose of TRH increased social play. Two monkeys showed repetitive, stereotyped behaviors even in baseline observations, and certain doses of TRH and MIF may have increased the frequency of these behaviors.

Animals↗
PubMed1980

MSH and MIF-I in animal models of tardive dyskinesia.

alpha-Melanocyte stimulating hormone (MSH) and MSH release inhibiting factor (MIF-I) were tested for their effects on animals with prior exposure to haloperidol. Such animals are known to have an augmented sterotypic response to dopamine agonists and have been used as an animal model of tardive dyskinesia. Both MSH and MIF-I increased the stereotypy that followed the administration of the lowest dose of apomorphine (0.125 mg/kg), suggesting that MSH and MIF-I might weakly increase dopaminergic transmission.

Animals↗
PubMed1982

Failure of MIF-1 or naloxone to reverse ischemic-induced neurologic deficits in gerbils.

MIF-1 and naloxone exert similar actions in several situations. Since naloxone, at a dose of 1 mg/kg IP, has been reported to reverse the neurologic deficits of gerbils whose right common carotid artery had been occluded, MIF-1 was tested under the same conditions and the effects compared with naloxone. Doses of 0.1, 1.0, and 10.0 mg/kg IP of MIF-1 and naloxone did not significantly alter the signs of either moderate or severe neurologic deficits. Thus, the results of this study with gerbils do not add evidence for the use of these opiate antagonists in strokes.

Animals↗
PubMed1984

MIF-1 (Pro-Leu-Gly-NH2) decreases activity in Siamese fighting fish (Betta splendens).

The effects of MIF-1 (Pro-Leu-Gly-NH2) on activity and aggression of male Siamese Fighting Fish ( Betta splendens) were considered. Animals were given intraperitoneal injections of 0.0 or 10.0 mg/kg MIF-1. After a 10-minute delay, they were placed in a 10 gallon aquarium and their activity was monitored for 60 minutes. Although aggressive responses in the presence of suitable opponents were not reliably affected, as significant decrease in general activity was produced. This is compatible with differential effects of MIF-1 across species.

Aggression↗
PubMed1985

Tyr-MIF-1, identified in brain tissue, and its analogs are active in two models of antinociception.

The antiopiate activities of Tyr-MIF-1 (Tyr-Pro-Leu-Gly-NH2) and some of its representative analogs were tested in two animal models of antinociception. Doses of the tetrapeptides as low as 0.001 mg/kg injected peripherally could block the analgesic effects of morphine in both the tail-flick test of mild thermal pain induced by heat and the scratching test of mild chemical pain induced by hypertonic saline. These tetrapeptides showed cross-reactivity in the radio-immunoassay (RIA) used to identify the presence of Tyr-MIF-1 in brain extracts and in the brain membrane binding assay. Only Tyr-MIF-1, however, eluted at the position of the immunoreactive peak after gel filtration chromatography and high performance liquid chromatography (HPLC). The results support the concept that peptides with anti-opiate activity can exist in the brain.

Analgesics, Opioid↗
PubMed1988

Naloxone, but not Tyr-MIF-1, reduces volitional ethanol drinking in rats: correlation with degree of spontaneous preference.

The possible relationship between the actions of ethanol and opiates led us to examine the effect of opiate antagonists on ethanol intake in rats with a free choice of water. Naloxone (NAL) significantly reduced intake of ethanol. This effect was much greater in "high-preferring" (ethanol/total fluid intake greater than 60%) than in "low-preferring" (ethanol/total fluid intake less than 30%) rats. Furthermore, a correlation was found between the degree of spontaneous preference (ethanol/total fluid intake ratio) and the reduction of ethanol drinking by NAL. Sensitivity to NAL increased with increased preference for ethanol. Neither Tyr-MIF-1 (Tyr-Pro-Leu-Gly-NH2) nor MIF-1 (Pro-Leu-Gly-NH2) caused a significant modification of ethanol intake. This study shows that NAL can reduce volitional ethanol intake in rats and provides further evidence that Tyr-MIF-1 does not always act like NAL.

Alcohol Drinking↗
PubMed1993

Isolation of Tyr-W-MIF-1 from bovine hypothalami.

Tyr-W-MIF-1 (Tyr-Pro-Trp-Gly-NH2) was recently isolated from human brain cortex. We have now isolated it from bovine hypothalami by solid phase extraction and several consecutive rpHPLC steps monitored by an RIA originally developed for the endogenous brain peptide Tyr-MIF-1 (Tyr-Pro-Leu-Gly-NH2). Determination of the sequence of the purified material and comparison of its chromatographic behavior with synthetic Tyr-W-MIF-1 confirmed the structure. The synthetic peptide and the isolated material showed almost identical binding to mu opiate receptors.

Amino Acid Sequence↗
PubMed1988

Colon cancer bearing rats produce a lymphokine which induces macrophage migration inhibition (MIF) in vitro.

We studied a series of 40 rats at various stages of colorectal carcinoma, as induced by N-methyl-N-nitro-Nitrosoguanidine. Lymphokine containing supernatants were obtained simultaneously from splenic and peripheral lymphocytes, after exposure to rat colon cancer antigen in vitro. The lymphokine was found capable of performing Macrophage Migration Inhibition (MIF) when obtained from rats with: carcinoma through serosa, carcinoma of submucosa, carcinoma of the mucosa and carcinoma in situ. All control rats were free of cancer and were MIF negative. The MIF response in this study was evaluated as a marker of chemically induced colorectal carcinoma in rats in order to better understand the lymphocyte response to tumor progression from atypia to adenocarcinoma of the colon.

Adenocarcinoma↗
PubMedDate not supplied

Sex differences in naloxone- and Tyr-MIF-1-induced hypoalgesia.

Reproductive adult male and female deer mice that received daily (7 days) injections of either the prototypic exogenous opiate antagonist, naloxone (1.0 mg/kg), or the endogenous putative antiopioid tetrapeptide, Tyr-MIF-1 (Tyr-Pro-Leu-Gly amide; 1.0 and 10 mg/kg), followed by determinations of thermal nociceptive sensitivity (hot-plate response) developed hypoalgesia. There were significant sex differences in this opioid blockade-induced or associated analgesia, with male mice displaying significantly greater hypoalgesia than females. Mice that received daily injections of either naloxone or Tyr-MIF-1 for 7 days without any accompanying determinations of nociceptive sensitivity (days 2-6 of treatment) failed to show any hypoalgesia on day 7 when they received the antagonist followed by a measurement of nociception. These results indicate that there are sex differences in both naloxone- and Tyr-MIF-1-induced hypoalgesia, and suggest that this pattern may be associated with sexually dimorphic opioid modulation of aversive conditioning.

Animals↗
PubMed1996

Periventricular penetration and disappearance of ICV Tyr-MIF-1, DAMGO, tyrosine, and albumin.

The penetration of four radioiodinated materials-Tyr-MIF-1, DAMGO, tyrosine, and albumin-into the periventricular tissue after ICV injection was studied in rats by film autoradiography. Rates of disappearance from the CNS for the injected compounds were also determined by computer-assisted image analysis of the autoradiographic images. The four materials showed distinct patterns of dispersion from the ventricular system, with Tyr-MIF-1 moving farthest into the parenchyma of the brain and albumin primarily restricted to the ventricular space. The other two compounds, tyrosine and DAMGO, had intermediate values. Tyr-MIF-1 also displayed the fastest rate of removal from the brain, which may represent the ability of the peptide to gain access to sites of saturable transport. By contrast, the exit from the brain of DAMGO was minimal, whereas the efflux of albumin and tyrosine was intermediate. These results show the utility of these methods in the simultaneous measurement of both the patterns of distribution within the CNS and the rates of removal from the CNS of compounds injected into the brain.

Albumins↗
PubMed1994

Saturable efflux of the peptides RC-160 and Tyr-MIF-1 by different parts of the blood-brain barrier.

Peptides have been shown to be transported in the direction of both blood to brain and brain to blood. Although blood to brain transport is known to occur at both the choroid plexus and the capillary bed of the brain, comprising the two major components of the blood-brain barrier, the location of efflux systems for peptides remains largely unstudied. We adapted established methodologies to study this question for two peptides known to be transported out of the brain after injection into the cerebrospinal fluid (CSF): Tyr-MIF-1, transported by peptide transport system (PTS)-1 and RC-160, a somatostatin analog transported by PTS-5. Radioactive iodide, known to be transported out of the brain primarily by the capillaries, also was studied. We found that after injection into brain tissue, RC-160 and iodide were rapidly transported out of the brain by saturable mechanisms. By contrast, efflux of Tyr-MIF-1 was slow and nonsaturable after injection into brain tissue, but rapid and saturable after injection into the lateral ventricle of the brain. Autoradiography confirmed that peptide injected into brain tissue did not diffuse far from the site of injection during the study period. The results indicate that the efflux system for RC-160 is located at least partly at the capillaries and suggest that the major location for the efflux system of Tyr-MIF-1 is at the choroid plexus.

Analgesics↗
PubMed2004

Re-examining the oligomerization state of macrophage migration inhibitory factor (MIF) in solution.

The state of oligomerization of macrophage migration inhibitory factor (MIF, also known as glycosylation inhibiting factor, GIF) in solution has been variously reported as monomer, dimer, trimer, or mixtures of all three. Several crystal structures show MIF to be a trimer. Sedimentation velocity shows a recombinant human MIF sample is quite homogeneous, with 98% as a species with s(20,w)=3.07 S and D(20,w)=8.29 x 10(-7) cm(2)/s. Using the partial specific volume calculated from the amino acid composition these values imply a mass of 33.56 kDa, well above that of dimer, but also 9% below the trimer mass of 37.035 kDa. Sedimentation equilibrium data at loading concentrations from 0.01 to 1 mg/ml show unequivocally that the self-association is extremely tight. However, the apparent mass is 33.53 kDa [95% confidence 33.25-33.82], again 9% below that expected for 100% trimer. To examine the possibility this protein has an unusual partial specific volume, sedimentation equilibrium was also done in H(2)O/D(2)O mixtures, giving 0.765+/-0.017 ml/g rather than the calculated 0.735 ml/g. With this revised partial specific volume, the equilibrium and velocity data each give M=37.9+/-2.8 kDa, fully consistent with a strongly-associated trimeric quaternary structure.

Crystallography, X-Ray↗
PubMed2006

Role of MIF and glutathione, in association with fetal ovine globin chain (Hbgamma) and LPS, in induction of TNFalpha from cells of young and aged mice, and PBL from healthy human populations.

Previous reports from our group have established that the fetal ovine gamma globin chain (Hbgamma) and LPS can synergize in the induction of pro-inflammatory cytokines, especially TNFalpha, from mouse and human leukocytes. A fetal sheep liver extract (FSLE) which was observed to have marked immunoregulatory properties in vivo and in vitro had independently been observed to contain significant amounts of each of these molecules. However, the biological activity of this extract (hereafter FSLE) was not explained solely by its content of Hbgamma and LPS, and independent analysis confirmed also the presence of migration inhibitory factor, MIF, and glutathione in FSLE. We have investigated whether MIF and the cellular anti-oxidant glutathione can further synergize with Hbgamma and LPS in TNFalpha induction from human cells in vitro, and mouse cells activated in vivo/in vitro. Our data show that indeed there is evidence for such a synergy. Treatment or mouse cells with FSLE produced an enhanced TNFalpha production which could be inhibited independently both by anti-Hbgamma and by anti-MIF, and optimally by a combination of these reagents.

Aging↗
PubMed1997

Immunohistochemical localization of macrophage migration inhibitory factor (MIF) in tanycytes, subcommissural organ and choroid plexus in the rat brain.

We investigated the immunohistochemical localization of the macrophage migration inhibitory factor (MIF) in the rat brain. In addition to epithelial ependymal cells lining the ventricular wall, tanycytes in the basomedial hypothalamus were heavily immunostained. The immunoreactive processes of tanycytes made contacts to sinusoidal capillaries and reached the pial surface forming an immuno-positive structure at the floor of the hypothalamus. Other immunoreactive cells contained the subcommissural organ in the roof of the third ventricle and the epithelial lamina of the choroid plexus. The localization of MIF in cells which have contact with cerebrospinal fluid and blood vessels suggests that MIF might play a role as a humoral factor in the brain.

Animals↗
PubMed1997

The macrophage migration inhibitory factor MIF is a phenylpyruvate tautomerase.

A macrophage migration inhibitory factor (MIF), originally described as a product of activated lymphocytes, has been defined as a 12 kDa protein, expressed in a wide variety of tissues. Here MIF is identified as a phenylpyruvate tautomerase (EC 5.3.2.1) having p-hydroxyphenylpyruvate and phenylpyruvate as its natural substrates. The definition of MIF as an enzyme may yield insight into the mechanism of action of this proinflammatory and immunomodulating cytokine.

Amino Acids↗
PubMed1982

Interaction of Lotus-tetragonolobus Lectin (LTL) and an MIF-like factor with guinea-pig macrophages. I. Effects on macrophage migration inhibition and receptor-binding studies.

Purified Lotus-tetragonolobus lectin (LTL) was studied for its interaction with guinea-pig peritoneal macrophages in the migration-inhibition and spreading-inhibition assay. LTL was found capable of inhibiting macrophage migration in a dose-response relationship similar to that of an MIF-life factor present in rat Zajdela-hepatoma ascites, whereas macrophage spreading was less affected. Mitogenic activity of the fucolectin could be excluded. Both the LTL and MIF-like factor seem to come into action by means of alpha-L-fucopyranosyl residues-containing macrophage surface receptors. Both substances act synergistically in inhibiting migration of macrophages. Since binding studies with 125I-LTL demonstrated competition with the MIF-like factor, it is suggested that the latter and LTL share a common surface receptor, and that optimal occupation densities are required for the realization of the inhibitory effect. Possibly, LTL acts in a monomeric form in the migration inhibition assay.

Animals↗
PubMed1999

Effects of neonatal treatment with Tyr-MIF-1 and naloxone on the long-term body weight gain induced by repeated postnatal stressful stimuli.

Stressful stimuli repeatedly applied during the first postnatal weeks can induce body weight gain in the mouse during adulthood. This effect can be prevented by injecting naloxone concomitantly with stress. The peptides belonging to the Tyr-MIF-1 family have a great modulating activity on numerous stress-induced phenomena. The aim of the present work was to compare the effect of repeated neonatal injections of Tyr-MIF-1 or naloxone on the long-term body weight gain induced by a stressing procedure applied daily during the first three weeks of life. The results indicate that although naloxone blocked the development of the stress-induced effects, Tyr-MIF-1 potentiated them.

Adipose Tissue↗
PubMed1995

MIF as a glucocorticoid-induced modulator of cytokine production.

Glucocorticoid hormones are important for vital functions and act to modulate inflammatory and immune responses. Yet, in contrast to other hormonal systems, no endogenous mediators have been identified that can directly counter-regulate their potent anti-inflammatory and immunosuppressive properties. Recent investigations of the protein macrophage migration inhibitory factor (MIF), which was discovered originally to be a T-lymphocyte-derived factor, have established it to be a pro-inflammatory pituitary and macrophage cytokine and a critical mediator of septic shock. Here we report the unexpected finding that low concentrations of glucocorticoids induce rather than inhibit MIF production from macrophages. MIF then acts to override glucocorticoid-mediated inhibition of cytokine secretion by lipopolysaccharide (LPS)-stimulated monocytes and to overcome glucocorticoid protection against lethal endotoxaemia. These observations identify a unique counter-regulatory system that functions to control inflammatory and immune responses.

Animals↗