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PubMedDate not supplied

Pharmacological activities of the MIF-1 analogues Pro-Leu-Gly, Tyr-Pro-Leu-Gly and pareptide.

The pharmacological activities of the related free acid analogues of MIF-1, Pro-Leu-Gly (PLG) and Tyr-Pro-Leu-Gly (YPLG), were investigated because of the possibility that they may be formed during the digestion of milk and wheat proteins in vivo. The amino acid sequences -Tyr-Pro-Leu-Gly- and -Pro-Leu-Gly- are present in proteins from these foods. Chronic administration of either PLG (0.25 mg/kg, SC, BID) or the control substance, pareptide (0.25 mg/kg, SC, BID), antagonized the development of tolerance to the cataleptic effects of haloperidol in mice. The effect of YPLG (0.25 mg/kg, SC, BID) on the development of this tolerance was borderline and not statistically significant. Nanomolar concentrations of PLG, YPLG, and pareptide each increased the in vitro binding of 3H-apomorphine to rat striatal receptors. In this in vitro system, bell-shaped dose response curves were observed for each peptide. The effects of these peptides on tolerance development and apomorphine binding are similar to those previously reported for MIF-1 and demonstrate that amidation at the carboxyl terminus is not required for biological activity.

Animals↗
PubMedDate not supplied

MIF-1 can accelerate neuromotor, EEG and behavioral development in mice.

Newborn mice were injected SC daily with 1 mg/kg of MIF-1 or saline during the first 19 days of life. The progress of each pup was monitored for physical (body weight, eye and ear opening), neurobehavioral (reflexes) and neurophysiological (EEG) development until the weaning stage. In early adulthood (40 days of age) mice were tested on a maze learning task. Results indicate that MIF-1 can accelerate neurologic (days 3-9), somatic (days 10-14) and electroencephalographic (days 16-19) parameters, and that the effects of treatment last into the early adult stage with increased learning abilities in an appetitive task.

Amino Acid Sequence↗
PubMed1994

Cyclic analogues of Tyr-W-MIF-1 with prolonged analgesic activity and potency comparable to DAMGO and morphine.

Two cyclic analogues of the brain peptide Tyr-W-MIF-1 (Tyr-Pro-Trp-Gly-NH2) were synthesized and tested for analgesic activity in the rat tail flick test after intracerebroventricular (ICV) injection. The analogues were about 200-fold more potent than the parent peptide. Analgesia was dose dependent, and at 1 microgram the two analogues, the mu-selective enkephalin analogue DAMGO (Tyr-D-Ala-Gly-N-Me-Phe-Gly-ol), and morphine, all produced analgesia lasting between 40 and 60 min. Analgesia of longer duration was evident at higher doses of the analogues and lasted more than 6 h after 100 micrograms, the highest dose tested. The results show that peptide analogues based on the structure of the endogenously occurring Tyr-W-MIF-1 can produce potent and long-lasting effects on nociception.

Analgesia↗
PubMed1988

Differential activity of the endogenous antiopiate Tyr-MIF-1 after various intensities of stress.

Three forms of stress-induced analgesia (electric shock, forced water-swim and novelty) were used to examine the nature of the endogenous antiopiate system. It was hypothesized that a role of the antiopiate system may be to regulate the extent of antinociception within varying environments. The antiopiate properties of Tyr-MIF-1 (Tyr-Pro-Leu-Gly-NH2), which were manifest by reduction of opiate analgesia in mice on a hot-plate, were best expressed within a defined range of intensities. In each of the 3 analgesic situations, pre-administration of Tyr-MIF-1 (0.1 mg/kg) resulted in an antinociceptive effect after low to moderate stress but not after more intense stress. These observations indicate that the antiopiate system can function differentially under various environmental conditions, thus ensuring that the organism's responses to its perception of the immediate environment are appropriate and specific.

Analgesia↗
PubMed1993

Prolonged analgesia after intracerebroventricular Tyr-W-MIF-1 (Tyr-Pro-Trp-Gly-NH2).

A peptide recently isolated from human and bovine brain, Tyr-W-MIF-1 (Tyr-Pro-Trp-Gly-NH2), was tested for its effects on nociception in the tail-flick test after intracerebroventricular injection in the rat. Tail-flick latencies were significantly increased with a rapid onset and remained significantly elevated for at least 50 min. Naloxone reversed the effect of the peptide, indicating opiate receptor involvement in the response. Met-enkephalin at the same dose produced only slight antinociception. Some animals showed 'barrel-rolling' behavior in addition to the analgesia; this behavior was unusually short-lived, not a prerequisite for the analgesia, and had no apparent persistent effects. The results show that, in addition to previously described opiate-like actions (binding to the mu-receptor and inhibition of electrically induced contractions of the guinea pig ileum), Tyr-W-MIF-1 is capable of inducing significant analgesia.

Amino Acid Sequence↗
PubMed1985

Developmental, behavioral, and opiate receptor changes after prenatal or postnatal beta-endorphin, CRF, or Tyr-MIF-1.

Developmental and long-term behavioral effects of perinatal injection of beta-endorphin (BE), CRF and Tyr-Pro-Leu-Gly-NH2 (Tyr-MIF-1) in male rats were investigated along with the possibility that opiate receptors may be altered by the injection of BE during this critical time. Daily injections of peptide were given to pregnant females (100 micrograms/rat) in the week before birth or to the offspring (50 micrograms/rat) of untreated mothers during the first week of life. Prenatal BE and CRF reduced body weight on day 1, in contrast to Tyr-MIF-1 which produced a significant increase over controls by day 7 as well as a slight but significant acceleration of eye opening. Among the postnatal treatments, CRF-treated animals showed the most dramatic changes. These included decreased body weight, accelerated eye opening, and, in adulthood, increased open field rearing behavior and a tendency for a monotonic body temperature response to low doses of morphine, in contrast to the biphasic response shown by controls. BE, when given to pregnant mothers, increased the number (Bmax) of [3H]naloxone-labeled (mu) receptors in whole brains of offspring assayed on day 14, but it did not significantly alter [3H]D-Ala-D-Leu-enkephalin-labeled (delta) receptors. In contrast, a significant decrease in both mu and delta receptors was observed on day 14 in rats given BE postnatally. These differences in receptors were no longer apparent in adulthood, and no significant differences in tail-flick response were detectable at this time. Nevertheless, some of the effects of these three peptides endured well beyond their presence, and for BE included changes in the number of opiate receptors.

Animals↗
PubMed1995

Enhanced isolation of Tyr-MIF-1 from fresh human brain cortex.

Tyr-MIF-1 previously was isolated from tissue obtained after death. A possible role of autolysis could not be excluded. We report the isolation of Tyr-MIF-1 (Tyr-Pro-Leu-Gly-NH2) in increased amounts from fresh human brain cortex. This confirms the natural existence of this brain peptide.

Cerebral Cortex↗
PubMed2006

Critical modifications of the ISO-1 scaffold improve its potent inhibition of macrophage migration inhibitory factor (MIF) tautomerase activity.

Based on the scaffold of (S,R)-3-(4-hydroxyphenyl)-4,5-dihydro-5-isoxazole acetic acid methyl ester (ISO-1), an inhibitor of the proinflammatory cytokine MIF, two critical modifications and chiral resolution have significantly improved the potency of the inhibition. Compound (R)-17 is 20-fold more potent than ISO-1 and inhibits MIF tautomerase activity with an IC(50) of 550 nM.

Enzyme Inhibitors↗
PubMed2006

Characterization of patterns of expression of protein kinase C-alpha, -delta, -eta, -gamma and -zeta and their correlations to p53, galectin-3, the retinoic acid receptor-beta and the macrophage migration inhibitory factor (MIF) in human cholesteatomas.

Cholesteatoma is a benign disease characterized by the presence of an unrestrained growth and the accumulation of keratin in the middle ear cavity. Due to roles in cell proliferation, apoptosis and differentiation members of the protein kinase C (PKC) family could be involved in disease progression. This study focuses on the expression of protein kinase C-alpha, -delta, -eta, -gamma and -zeta in the epithelial tissues of 56 human cholesteatomas and their correlations with those of previously characterized distributions of p53, galectin-3, retinoic acid receptor-beta (RARbeta) and macrophage migration inhibitory factor (MIF). We have previously reported this marker set to be correlated with keratinocyte differentiation in human cholesteatomas. Our present data clearly show that the percentage of PKC-alpha (but not PKC-delta, -gamma, -eta and -zeta)-immunopositive cells in epithelial tissue fro recurrent cholesteatomas was significantly higher than in non-recurrent cases. Correlations between the PKC isoenzymes and the biological markers were non-uniform. PKC-alpha (but not PKC-delta, -gamma, -eta and -zeta) expression in epithelial cholesteatoma cells correlated significantly and positively with the percentages of p53-immunopositive cells. The patterns of PKC-alpha and -delta expression, but not of PKC-gamma, -eta and -zeta, correlated significantly and positively with galectin-3 expression. In addition, the correlation levels between the expression of PKC-alpha and -delta and that of galectin-3 varied depending on the infection and recurrence status. Presence of RARbeta correlated significantly (and positively) with the expression of PKC-gamma and -zeta and also in relation to the infection and recurrence status. MIF correlated presence significantly (and positively) with that of the five PKCs under study, depending on whether the cholesteatomas were non-infected or infected as well as non-recurrent or recurrent. In conclusion, the present study suggests that modifications occurring at the level of keratinocyte differentiation in human cholesteatomas involve distinct effectors, to which the activation of PKC-alpha, -delta, -eta, -gamma and -zeta can be added.

Adolescent↗
PubMed2003

The apoptosis-associated protein BNIPL interacts with two cell proliferation-related proteins, MIF and GFER.

Bcl-2/adenovirus E1B 19 kDa interacting protein 2-like, BNIP-2-like (BNIPL) is a recently cloned and characterized apoptosis-associated protein that shares 72% homology with BNIP-2. It is highly expressed in human placenta and lung. A yeast two-hybrid system was used to obtain two BNIPL-interacting proteins, MIF (macrophage migration inhibitory factor) and GFER (growth factor erv1 (Saccharomyces cerevisiae)-like). The interactions were confirmed by glutathione S-transferase pull-down assay in vitro and co-immunoprecipitation assay in vivo. Colony formation assay and cell proliferation test suggest that overexpression of BNIPL could inhibit the growth of BEL-7402 cells. These findings suggest that BNIPL may physically bind to cell proliferation-related proteins, MIF and GFER.

Adaptor Proteins, Signal Transducing↗
PubMed1996

Opioid binding profile of morphiceptin, Tyr-MIF-1 and dynorphin-related peptides in rat brain membranes.

Opioid properties of several morphiceptin- (Tyr-Pro-Phe-Pro-NH2), Tyr-MIF-1 (Tyr-Pro-Leu-Gly-NH2) and dynorphin-derivatives were characterized in rat brain in vitro receptor binding assay and in electrically stimulated longitudinal muscle strip preparation of guinea pig ileum. In the case of morphiceptin-related peptides, an excellent correlation was found between the [3H]-naloxone binding displacement data and the agonist potencies determined in the bioassay. The "turning point' was the C-terminal amidation in the tri- and tetrapeptide pairs in both series. Tyr-MIF-1 derivatives showed weak affinity in the opioid receptor binding assay and none of them had any remarkable effect in the bioassay either as agonist or antagonist. The dynorphin A(1-10)-peptides modified at positions 5 and 8 retained their affinity with Pro5-, Pro8-, and Ala8-substituents, whereas some loss of affinity was observed in the case of Gly8-Dyn A(1-10).

Analgesics↗
PubMed1981

Selective effects of alpha-MSH and MIF-1 on the blood-brain barrier.

The effects of intravenously-injected alpha-MSH and MIF-1 (Pro-Leu-Gly-NH2) on the permeability of the blood-brain barrier (BBB) to a large protein and a small anion were studied using radioiodinated serum albumin (RISA) and 99mTc-labeled sodium pertechnetate. The permeability of the BBB to RISA was unaltered by either peptide. Permeability to the inorganic pertechnetate anion, however, was significantly increased by alpha-MSH but not by MIF-1 at doses known to evoke EEG and behavioral responses. The peptides did not cause a change in the systemic blood pressure. It is possible, therefore, that at least some CNS effects of peripherally administered peptides are exerted by alteration of the permeability of the BBB to other substances.

Animals↗
PubMed1998

DNA sequence motifs are associated with aberrant homologous recombination in the mouse macrophage migration inhibitory factor (Mif) locus.

Homologous recombination is a precise genetic event that can introduce specific alteration in the genome. A planned targeted disruption by homologous recombination of the macrophage migration inhibitory factor (Mif) locus in mouse embryonic stem (ES) cells yielded the targeted clones, some of which had genomic rearrangements inconsistent with the expected homologous recombination event. A detailed characterization of the recombination breakpoints in two of these clones revealed several sequence motifs with possible roles in recombination. These motifs included short regions of sequence identity that may promote DNA alignment, multiple 5'-AAGG/TTCC-3' tetrameres, topoisomerase I consensus sites, and AT-rich sequences that can promote DNA cleavage and recombination. A retrovirus-like intracisternal-A particle (IAP) family sequence was also identified upstream of the Mif gene, and the LTR of this IAP was involved in one of the recombinations. Identification and characterization of such sequence motifs will be valuable for the gene targeting experiments.

Adenine Nucleotides↗
PubMed2002

Macrophage migration inhibitory factor (MIF): mechanisms of action and role in disease.

Macrophage migration inhibitory factor (MIF) is a unique cytokine and critical mediator of host defenses with a role in septic shock and chronic inflammatory and autoimmune diseases. Its mechanism of action is incompletely understood. Here, we attempt to correlate current knowledge on the molecular pathways of MIF activity with its functions in immunity and disease.

Animals↗
PubMed2004

Analysis of chicken TLR4, CD28, MIF, MD-2, and LITAF genes in a Salmonella enteritidis resource population.

Salmonella enteritidis is a foodborne pathogen that negatively affects both animal and human health. Genetic variations in response to pathogenic SE colonization or to SE vaccination were measured in a chicken resource population. Outbred broiler sires and 3 diverse, highly inbred dam lines produced 508 F1 progeny that were evaluated for either bacterial colonization after pathogenic SE inoculation or circulating antibody level after SE vaccination. Five candidate genes were selected for study, based on their biological function as possibly affecting response to SE: toll-like receptor 4 (TLR4), T-cell specific surface protein (CD28), macrophage migration inhibitory factor (MIF), MD-2, and lipopolysaccharide-induced tumor necrosis factor (TNF)-alpha factor (LITAF). Gene fragments were sequenced from the founder lines of the resource population. The LITAF and MIF genes were homozygous for all sires. Single nucleotide polymorphisms (SNP) were identified in 3 genes (TLR4, CD28, and MD-2) and were used to test for associations of sire SNP with SE response. Linear mixed models were used for statistical analyses. The CD28 broiler sire SNP was associated with both bacterial load in the cecum (P < 0.003) and vaccine antibody response (P < 0.05). The MD-2 SNP was associated (P < 0.04) with the bacterial load in the spleen. The use of these SNP in these genes in marker-assisted selection may result in enhancement of disease resistance.

Animals↗
PubMed2002

Endomorphins, Met-enkephalin, Tyr-MIF-1, and the P-glycoprotein efflux system.

The P-glycoprotein (P-gp) transport system, responsible for the efflux of many therapeutic drugs out of the brain, recently has been shown to transport the endogenous brain opiate endorphin. We used P-gp knockout mice (Mdr1a) and their controls to determine where P-gp is involved in the saturable efflux systems of four other endogenous opiate-modulating peptides across the blood-brain barrier (BBB). After injection of endomorphin-1 (Tyr-Pro-Trp-Phe-NH(2)), endomorphin-2 (Tyr-Pro-Phe-Phe-NH(2)), Met-enkephalin (Tyr-Gly-Gly-Phe-Met-OH), and Tyr-MIF-1 (Tyr-Pro-Leu-Gly-NH(2)) into the lateral ventricle of the mouse brain, residual radioactivity was measured at 0, 2, 5, 10, and 20 min later. The results showed no difference in the disappearance of any of these peptides from the brains of knockout mice compared with their controls. This demonstrates that unlike endorphin and morphine, P-gp does not seem to be required for the brain-to-blood transport of the endomorphins, Met-enkephalin, or Tyr-MIF-1 across the BBB.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2002

Expression of selected apoptosis related genes, MIF, IGIF and TNF alpha, during retinoic acid-induced neural differentiation in murine embryonic stem cells.

Apoptosis plays an important role during embryonic development. Apoptotic cell death is executed by caspases and can be regulated by the Bcl-2 family of genes. Ribonuclease protection assay was used to investigate the expression of selected apoptosis-related genes of the Bcl-2 family, pro-apoptotic Bax, Bad and anti-apoptotic Bcl-2, during differentiation of murine embryonic stem cells (ES) mediated by all-trans-retinoic acid. The mRNA expression of caspase 3, caspase 6 and certain pro-inflammatory cytokines was also investigated simultaneously. ES cells exposed to 1 microM all-trans-retinoic acid on day 8, 9 and 10 of differentiation revealed increased expression of Bax and Bad compared to the vehicle-treated cells. No effect on Bcl-2 mRNA was noted after all-trans-retinoic acid treatment. Increased mRNA expression of caspase 3 and caspase 6 in all-trans-retinoic acid-exposed ES cells suggested that caspases play an important role in retinoic acid-mediated apoptosis during ES differentiation. Increase in the expression of TNF alpha and macrophage migration inhibitory factor (MIF) was noted in retinoic acid-treated cells on day 14. Significant increase observed in interferon gamma inducing factor (IGIF/IL-18) mRNA expression in all-trans-retinoic acid-treated cells on day 14 and 17 did not translate to increased INF gamma expression. No change in the expression of other pro-inflammatory cytokines was noted with all-trans-retinoic acid treatment. The function of TNF alpha, IGIF/IL-18 and MIF in all-trans-retinoic acid-treated cells during ES differentiation and apoptosis is still speculatory. Results suggested that RA-mediated apoptosis during neural differentiation of ES cells involves up-regulation of caspase 3, caspase 6, Bad, and Bax.

Animals↗
PubMedDate not supplied

Leucocyte migration inhibition factor (L-MIF) in malnourished Nigerian children.

Leucocyte Migration Inhibition Factor (L-MIF) was measured in 41 children with marasmus, 19 with kwashiorkor, 5 with marasmic-kwashiorkor and 35 well-fed healthy children serving as controls. For L-MIF assay, two different antigens (live attenuated measles virus vaccine and diptheria pertussis tetanus (DPT) vaccine were used. Percentage migration indices obtained with the two antigens were significantly higher in the malnourished than in the well-fed healthy sex and age-matched controls (P < 0.01). The total serum protein and albumin concentrations were significantly reduced in the malnourished children compared with the controls (P < 0.01). Mean total leucocyte numbers were not significantly different in marasmic and marasmic-kwashiorkor children compared with the controls (P > 0.21).

Blood Proteins↗