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PubMed1992

Age- and sex-related changes in Tyr-MIF-1-like immunoreactivity in rat plasma.

The concentrations in plasma of the biologically active endogenous peptide Tyr-MIF-1 (Tyr-Pro-Leu-Gly-NH2) have not been measured during development or in female rats. By radioimmunoassay, we found that Tyr-MIF-1-like immunoreactivity (Tyr-MIF-1-LI) was first consistently detectable in plasma when the rat was 5 days old, and then gradually increased to adult concentrations by day 15. In male rats, the levels remained relatively constant for the next 21 months. In female rats, plasma concentrations of Tyr-MIF-1-LI at day 15 were about the same as in male rats. At 6 months of age, however, the concentrations in females decreased by half and by 21 months of life were only about a third of the concentrations found at day 15 or in age-matched males. The differences with age were not due to the length of time of storage of the samples, because another group of rats 1 month old was killed on the same day as 5-day-old rats and still showed several times more Tyr-MIF-1-LI in the plasma; again, no differences were found between male and female rats at either 5 days or 1 month. A single injection of estradiol followed by progesterone lowered the concentrations in 1-month-old male rats. In female rats that were either ovariectomized or sham-ovariectomized, the expected similarity in their plasma concentrations of Tyr-MIF-1-LI was found at 1 month of age.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Distribution↗
PubMed1990

The biological effects of XTC-MIF: quantitative comparison with Xenopus bFGF.

Mesoderm in Xenopus and other amphibian embryos is induced by signals from the vegetal hemisphere acting on equatorial or animal hemisphere cells. These signals are diffusible and two classes of candidate signal molecule have been identified: the fibroblast growth factor (FGF) and transforming growth factor beta (TGF-beta) types. In this paper, we compare the effects of cloned Xenopus basic FGF (XbFGF) and electophoretically homogeneous XTC-MIF (a TGF-beta-like factor obtained from a Xenopus cell line) on animal pole explants. We find that they have a similar minimum active concentration (0.1-0.2 ng ml-1) but that, nonetheless, XTC-MIF is at least 40 times more active in inducing muscle. In general, we find that the two factors cause inductions of significantly different characters in terms of tissue type, morphology, gene expression and timing. At low concentrations (0.1-1.0 ng ml-1) both factors induce the differentiation of 'mesenchyme' and 'mesothelium' as well as blood-like cells. These latter cells do not, however, react with an antibody to Xenopus globin. This raised the possibility that the identification of red blood cells in other studies on mesoderm induction might have been mistaken, but combinations of animal pole regions with ventral vegetal pole regions confirmed that genuine erythrocytes are formed. The identity of the blood-like cells formed in response to the inducing factors remains unknown. At higher concentrations XTC-MIF induces neural tissue, notochord, pronephros and substantial and often segmented muscle. By contrast, XbFGF only induces significant amounts of muscle above 24 ng ml-1 and even then this is much less than that induced by XTC-MIF. For both factors an exposure of less than 30 min is effective. Competence of animal pole cells to respond to XbFGF is completely lost by the beginning of gastrulation (stage 10) while competence to XTC-MIF is detectable until somewhat later (stage 11). Since animal pole tissue is known to be able to respond to the natural inducer at least until stage 10, and perhaps until stage 10.5, this suggests that bFGF cannot be the sole inducer of mesoderm in vivo. Taken together, these results are consistent with XTC-MIF being a dorsoanterior inducer and XbFGF a ventroposterior inducer, suggesting that body pattern is established by the interaction of two types of inducing signal. This model is discussed in view of the qualitative and quantitative differences between the factors.

Animals↗
PubMed1999

Effects of Tyr-MIF-1 on stress-induced analgesia and the blockade of development of morphine tolerance by stress in mice.

The role of Tyr-MIF-1 (Tyr-Pro-Leu-Gly-NH2) in biological responses to stress exposure was examined in mice. Intraperitoneal or intracerebroventricular administration of Tyr-MIF-1 attenuated not only footshock (FS)- and forced swimming (SW)-stress-induced analgesia (SIA) but also socio-psychological (PSY)-SIA that, when using the communication box, is produced without any direct physical nociceptions. Tyr-MIF-1 also disrupted the suppressive effect of concurrent exposure to FS- and PSY-stress on the development of morphine antinociceptive tolerance. In elevated-plus-maze tests, mice treated with Tyr-MIF-1 tended to spend more time in the open arms compared with the control group, suggesting the anxiolytic properties of the peptide. Thus, the finding that Tyr-MIF-1 modulates these stress responses suggests that the peptide regulates an endogenous biological alert system responding to stress exposure, perhaps, counteracting the excessive response of the system. Furthermore, Tyr-MIF-1, in the case of PSY-stress, through the attenuation of emotional factors such as fear and anxiety, may suppress PSY-SIA and inhibition by PSY-stress of the development of morphine tolerance.

Analgesics, Opioid↗
PubMed1976

Dissociation of MIF activity and in vitro lymphocyte transformation in the development of experimental allergic thyroiditis in guinea pigs.

Macrophage migration inhibitory factor (MIF) activity and in vitro lymphocyte transformation to homologous thyroid antigen were compared in cultures of lymph node cells obtained from 123 guinea pigs at weekly intervals after a single injection of homologous thyroid extracts in complete Freund's adjuvant (CFA). MIF activity was not detectable at the early stage of immunization but became manifest 2 and 3 weeks after sensitization and a high level was maintained during 4-7 weeks. On the other hand, lymphocyte transformation preceded the appearance of MIF activity and attained its maximum 2 weeks after sensitization before the establishment of thyroiditis. It is indicated that MIF activity and lymphocyte transformation predominate separately in the course of immunization. There was a considerable correlation between intensity of MIF activity and severity of thyroiditis in individual animals during the advanced stage (4-6 weeks after sensitization) of the disease. Also, a lower but significant correlation was seen between lymphocyte transformation and severity of thyroiditis. However, about half of animals in the advanced stage of thyroiditis failed to exhibit antigen-stimulated lymphocyte transformation, despite a positive MIF activity.

Animals↗
PubMed1980

Antagonistic actions of MIF-I on the hypothermia and hypomotility induced by beta-endorphin or morphine.

Recently it has been suggested that MIF-I can act as an opiate antagonist for analgesia. Therefore, rats kept at 4 degrees C were pretreated with MIF-I in an attempt to extend the observation to a nonanalgesic opiate effect by determining any blockade of the thermal response to beta-endorphin and morphine. MIF-I, at an ip dose of 1.0 mg/kg, was found to block the thermal responses to beta-endorphin injected ip at doses of 0.1 and 1.0 mg/kg. A lower dose (0.1 mg/kg, ip) of MIF-I, or naloxone (10 mg/kg), was also able to block the thermal effects of 30 and 60 mg/kg doses of morphine. However, an ip dose of 1.0 mg/kg MIF-I potentiated the hypothermic effects of morphine but, like naloxone, reduced the magnitude of the decrease in the level of motor activity induced by beta-endorphin or by morphine. The results of this study demonstrate a nonanalgesic situation in which MIF-I can act as an antagonist of opiate effects after peripheral injection.

Animals↗
PubMed1999

Macrophage migration inhibitory factor (MIF)--its role in catecholamine metabolism.

Macrophage migration inhibitory factor (MIF) was originally identified several decades ago as a lymphokine-derived protein that inhibited monocyte migration. Recently, it has been reported that MIF has D-dopachrome tautomerase, phenylpyruvate tautomerase and thiol protein oxidoreductase activities, although the physiological significance of those activities is not yet clear. Here we show that MIF is able to catalyze the conversion of dopaminechrome and norepinephrinechrome, toxic quinone products of the neurotransmitters dopamine and norepinephrine, respectively, to indole derivatives that may serve as precursors to neuromelanin. Since MIF is highly expressed in human brain, these observations raise the possibility that MIF participates in a detoxification pathway for catecholamine products and could therefore have an important role for neural tissues. The potential role of MIF in the formation of neuromelanin from catecholamines is also an extremely interesting possibility.

Animals↗
PubMed1975

Studies on the production of MIF and mitogenic factor using highly purified human T and B lymphocytes.

Human lymphocytes were separated into highly purified populations using an immunoadsorbent column technique. It was previously reported that both T and B cells exhibited increased 3H-thymidine incorporation in response to PHA, Con A and pokeweed mitogens, whereas only T cells showed increased incorporation in response to specific antigen. In the present studies, the cellular basis of MIF and mitogenic factor production was studied. Both T and B cells produced MIF in response to antigen. The MIF produced by both T and B cells elutes from Sephadex G-100 columns in the same fraction. Studies using BUdR and light suggest that the T cell which produces MIF is also a proliferating cell, whereas the B cell producing MIF is not. Only T cells produce mitogenic factor in response to antigen. The mitogenic factor produced, however, causes both T and B cell populations to increase 3H-thymidine incorporation. The present studies indicate that antigen induced mitogenic factor production and increased 3H-thymidine incorporation are properties of T cells per se, whereas antigen-induced MIF is made by both T and B cells.

Antigens, Bacterial↗
PubMed1976

Lymphokines. II. Use of horse monocytes as indicator cells for human MIF.

Peritoneal exudate macrophages in guinea pigs and peripheral blood monocytes in man are the most readily available cells sensitive to the migration-inhibiting factor(s) (MIF) induced by tuberculin or insoluble concanavalin A in supernatants of stimulated lymphocyte cultures. The scarcity of MIF-sensitive cells is probably the main reason for the unsatisfactory results obtained with direct and indirect MIF tests when using white blood cells as indicator cells. Isolated horse monocytes represent an alternative sensitive source of indicator cells for human MIF assays, whereas guinea pig peritoneal exudate macrophages appear to be less sensitive and to show large individual variations in sensitivity to human MIF. The species specificity of MIF from various origins shows various patterns and is briefly discussed.

Animals↗
PubMed2006

[Distribution of MIF -173 single nucleotide polymorphism checked by tetra-primer amplification refractory mutation system].

OBJECTIVE: To study the distribution of macrophagemigration inhibitory factor gene (MIF) -173 single nucleotide polymorphism (SNP) of Chinese Han population in Zhejiang province. METHODS: The DNA samples were extracted from EDTA blood of 142 unrelated healthy individuals. Alleles of MIF -173 SNP were genotyped by using the techniques of tetra-primer amplification refractory mutation system (ARMS) and restriction fragment length polymorphisms (RFLP)-PCR Meantime the PCR products were cloned and sequenced. RESULTS: The authors detected three kinds of genotypes at the MIF -173 locus, and no deviation was observed from Hardy-Weinberg equilibrium. The final results were the same completely, whatever either tetra-primer ARMS or RFLP-PCR was used to check the MIF -173 single nucleotide polymorphism. Statistical analysis showed that the distributions of MIF -173 SNP alleles and genotype frequencies were significantly different between Chinese Han population and European Caucasian(P< 0.01), but no significant difference demonstrated to happen between Chinese and Japanese(P> 0.05). CONCLUSION: Tetra-primer ARMS is an accurate, rapid and economical method for SNP genotyping.There exists ethnic difference in the distribution of MIF -173 SNP alleles.

Adult↗
PubMed1996

Crystal structure of macrophage migration inhibitory factor (MIF), a glucocorticoid-induced regulator of cytokine production, reveals a unique architecture.

The mediator originally described as a macrophage migration inhibitory factor (MIF) has been identified recently to be a novel anterior pituitary hormone and the first protein to be released from immune cells upon stimulation with glucocorticoids. Once released, MIF acts to override or counter-regulate the immunosuppressive effects of glucocorticoids on cytokine production in vitro and on LPS lethality in vivo. MIF also has been described to catalyze a tautomerization reaction, suggesting that an enzymatic activity may underlie certain of its biological properties. The three-dimensional crystal structure of human MIF has been solved at 2.6A resolution. The X-ray crystal structure reveals MIF to be a trimer of identical subunits. Each monomer contains two antiparallel alpha-helices that pack against a four-stranded beta-sheet. The monomer has an additional two beta-strands that interact with the beta-sheets of adjacent subunits to form the interface between monomers. The three beta-sheets are arranged to form a barrel containing a solvent-accessible channel that runs through the center of the protein along a molecular three-fold axis. Electrostatic potential maps reveal that the channel has a positive potential, suggesting that it binds negatively charged molecules. The elucidated structure for MIF is unique among cytokines or hormones and suggests that this glucocorticoid-induced counter-regulatory hormone has a novel mechanism of action.

Animals↗
PubMed1998

Charge heterogeneity of macrophage migration inhibitory factor (MIF) in human liver and breast tissue.

Macrophage migration inhibitory factor (MIF) is an ubiquitous protein playing various immunological and hormonal roles. Theoretical electrophoretic coordinates calculated from protein sequence in the SWISS-PROT database (AC P14174) are 12 kDa and pI 8.24. Using two-dimensional (2-D) immunoblotting, we have detected isoelectric forms at ca. 11.9 kDa, with pI values of 7.8 and 6.98 in human liver tissue, breast tissue and a cell line and in preparations of human MIF expressed in E. coli. This evidence suggests that MIF charge heterogeneity originates from a post-translational modification not requiring eukaryote-specific enzymes. We have also detected in human liver a minor immunoreactive spot at pI 6.23, which coincides with the MIF spot in the liver map in SWISS-2DPAGE. The pI 6.23 isoform also conceivably derives from post-translational modification, as MIF is known to be encoded in the human genome by a single copy gene.

Amino Acid Sequence↗
PubMed1994

Cloning the human gene for macrophage migration inhibitory factor (MIF).

Macrophage migration inhibitory factor (MIF) was originally identified as a lymphokine. However, recent work strongly suggests a wider role for MIF beyond the immune system. It is expressed specifically in the differentiating cells of the immunologically privileged eye lens and brain, is a delayed early response gene in fibroblasts, and is expressed in many tissues. Here, we report the structure of the remarkably small gene for human MIF that has three exons separated by introns of only 189 and 95 bp and covers less than 1 kb. The cloned sequence also includes 1 kb of 5' flanking region. Primer extension and 5' rapid amplification of cDNA ends (RACE) of human brain RNA both indicate the presence of a single transcription start site in a TATA-less promoter. Northern blot analysis shows a single size of MIF mRNA (about 800 nt) in all human tissues examined. In contrast to previous reports, we find no evidence for multiple genes for MIF in the human genome.

Amino Acid Sequence↗
PubMedDate not supplied

Chlamydia trachomatis species specific serology: ImmunoComb Chlamydia bivalent versus microimmunofluorescence (MIF).

The ImmunoComb Chlamydia Bivalent IgG/IgA (Orgenics, Israel) is a new quantitative serologic test that employs LPS extracted Chlamydia trachomatis L2 and LPS extracted Chlamydia pneumoniae elementary bodies on two separate antigenic spots. The Bivalent C. trachomatis specific test results were compared with microimmunofluorescence (MIF), the gold standard of chlamydial species specific serology. For C. trachomatis IgG the Bivalent was highly concordant with the MIF: the rate of positive titres (IgG > or = 1:8) was 10% vs. 11% in 100 blood donors, 18% vs. 16% in 111 obstetric patients (6% antigen prevalence), 26% vs. 22% in sterile women with open (n = 54) and 86% vs. 84% with occluded (n = 51) tubes, and 88% vs. 85% in 103 women with C. trachomatis positive cervical smears. Surprisingly, the Bivalent differed considerably from the MIF in IgA prevalence: in obstetric patients (8% vs. 4%), sterile women with open (13% vs. 6%) and occluded (71% vs. 20%) tubes, and women with positive cervical smears (78% vs. 24%). Bivalent IgA appeared to be more sensitive than MIF IgA and showed a stronger correlation with positive cervical smears in obstetric patients (sensitivity 67% vs. 0%, specificity 95% vs. 96%, positive prediction 44% vs. 0%, negative prediction 98% vs. 94%) and with tubal occlusion in sterile women (sensitivity 71% vs. 20%, specificity 87% vs. 94%, positive prediction 84% vs. 77%, negative prediction 76% vs. 55%). MIF IgM was of little diagnostic help. Supplemental to the often difficult C. trachomatis antigen detection, the easily performed Bivalent IgG/IgA appears to be of great value in routine diagnosis of genital chlamydial infections.

Adult↗
PubMed1982

Macrophage migration inhibition factor (MIF): reducing the variables.

While the phenomenon of macrophage migration inhibition is a useful indicator of lymphokine release, it may be caused by other substances, it is subject to considerable variability, and it may be masked by the concomitant presence of substances stimulating migration. We have investigated certain aspects of the lymphokine macrophage interaction in order to circumvent these problems. Cells from the murine macrophage cell line RAW 264-7 migrated with less variability than fresh guinea pig peritoneal macrophages and were more sensitive target cells for human macrophage migration inhibition factor (MIF). Assays were performed with serum-free and endotoxin-free medium and in all cases in the presence and absence of L-fucose. This added specificity to the assay in that biological MIF activity was invariably blocked by L-fucose whereas migration inhibition produced by antigen complexed antibody, endotoxin, and periodate was not affected by L-fucose. It was also possible to demonstrate MIF activity in mixtures of MIF and migration stimulation factor by using L-fucose. We suggest that MIF activity is determined with less variability by using a macrophage cell line as indicator cells and performing the assays in the presence and absence of L-fucose.

Animals↗
PubMed1979

Effects of MIF-I and melatonin on novelty-induced defecation and associated plasma 11-OHCS and brain catecholamines.

In two experiments the effects were investigated of MSH-inhibiting factor-I (MIF-I) and of Melatonin on step-down latencies, defection, plasma 11-OHCS levels, whole brain DA and whole brain NE concentrations on Days 1, 3 and 5 of novelty exposure. Treatment with MIF-I led to a significant habituation of novelty-induced defecation over 5 days, whereas plasma 11-OHCS level was reduced only on Day 1. The concentrations of whole brain DA and whole brain NE also showed a significant increase over days of MIF-I and novelty treatment. Melatonin treatment, on the other hand, significantly inhibited novelty-induced defecation and reduced plasma 11-OHCS level on Day 5 of novelty exposure. Melatonin treatment led to a significant increase of whole brain DA in animals exposed to novelty for 5 days. Neither MIF-I nor Melatonin was found to significantly affect the step-down activity of treated animals. The overall results suggested a possible relationship between novelty-induced defecation and brain DA levels of MIF-I and Melatonin treated animals.

11-Hydroxycorticosteroids↗
PubMed1982

Effects of MIF-I, sex, and weight on tonic immobility in lizards (Anolis carolinensis).

Three experiments were done with the lizard, Anolis carolinensis, as a follow-up on our previous work which showed that MIF-I reduced tonic immobility (TI) during the breeding season and that females had longer TI durations than males in the non-breeding season. In June, during the breeding season, 60 male and 60 female lizards were injected with 0.1 mg/kg of MIF-I or naloxone or the diluent vehicle and placed in small aquaria for ten minutes. TI was then induced in the small aquaria. Similar experiments were conducted in September and October (non-breeding season). There was a reduction in TI durations in MIF-I and naloxone-treated lizards of both sexes in June, but the differences between drug treatment groups and controls were not significant. In September and October, MIF-I treatment resulted in TI durations similar to controls but naloxone treatment resulted in slightly shorter durations. Increased TI duration in females as compared to males was seen during both seasons, but diminished during the breeding season. Weight was found to be a factor in male lizards, with males greater than or equal to 4.0 g showing significantly longer TI durations. The lack of a significant effect of MIF-I on TI durations during the breeding season is possibly due to changes in the experimental design from the earlier report.

Animals↗
PubMed1987

Tyr-MIF-1 augments benzodiazepine receptor binding in vivo.

Behavioral and limited neurochemical evidence indicates possible links between the endogenous opiate and gamma-aminobutyric acid (GABA)-benzodiazepine receptor systems. A previous study using in vitro techniques indicated that MIF-1 (Pro-Leu-Gly-NH2) and Tyr-MIF-1 (Tyr-Pro-Leu-Gly-NH2), peptides with anti-opiate activity, enhanced GABA-stimulated benzodiazepine binding. To assess the activity of these peptides under in vivo conditions, we evaluated their effects on benzodiazepine receptor binding as determined by specific uptake of the benzodiazepine antagonist [3H]-Ro15-1788. Tyr-MIF-1, at a dose of 1 mg/kg IP, significantly augmented benzodiazepine binding in cortex and hippocampus but not in cerebellum, hypothalamus, or pons-medulla. Increases in binding were due in large part to increased apparent affinity at the receptor. At none of the doses of MIF-1 (0.1, 1 and 10 mg/kg) or at the highest (10 mg/kg) and lowest (0.1 mg/kg) doses of Tyr-MIF-1 was there any significant alteration in benzodiazepine binding in any region evaluated. These results indicate that peptide-benzodiazepine receptor interactions may also occur in vivo.

Animals↗
PubMedDate not supplied

Inhibition by MIF-I of alpha-MSH induced increase of intraocular pressure and miosis in rabbits.

The effects of intracameral (i.c.) administration of MIF-I on the ocular response to alpha-MSH were tested in rabbits. In confirmation of previous studies, i.c. alpha-MSH significantly increased intraocular pressure (IOP) and reduced pupillary diameter (PD). Concomitant administration of alpha-MSH and MIF-I antagonized both the IOP increase and miosis induced by alpha-MSH. Aqueous humor (AH) dynamics studies revealed that alpha-MSH increases IOP, possibly, by decreasing AH outflow. The decreased AH outflow induced by alpha-MSH was antagonized by concurrent administration of MIF-I and alpha-MSH. MIF-I did not affect IOP or PD when administered alone. These results add more support for a role of alpha-MSH in ocular function, and suggest that the ocular response to alpha-MSH may be subject to inhibitory control by MIF-I.

Animals↗