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PubMed1984

Three different activated ras genes in mouse tumours; evidence for oncogene activation during progression of a mouse lymphoma.

Five unrelated mouse tumours have been shown to carry activated transforming genes using the NIH/3T3 transfection assay. Three of these tumours, a T-cell lymphoma, a fibrosarcoma and a macrophage tumour, were found to carry an activated c-Ki-ras gene. A c-Ha-ras gene was shown to be activated in a myeloid leukaemia and a recently identified member of the 'ras' gene family, N-ras, was found to be activated in a lung carcinoma. The T-cell lymphoma, L5178Y-ES, is a more aggressively growing metastatic variant which arose spontaneously from the parental tumour, L5178Y-E. Although DNA from both parental and variant tumours was shown to transfer a genetic marker to recipient cells equally well, only the metastatic variant carried an activated c-Ki-ras gene detectable by transfection. The altered growth behaviour of the L5178Y-ES cells may therefore be the result of the spontaneous activation of the c-Ki-ras gene after the lymphoma cells had already become tumorigenic.

Animals↗
PubMed1986

Stage-specific changes in protein phosphorylation accompanying meiotic maturation of mouse oocytes and fertilization of mouse eggs.

Characteristic changes in the patterns of protein phosphorylation occur during meiotic maturation of mouse oocytes from the time subsequent to germinal vesicle breakdown, through metaphase II, and following fertilization. These changes occur during both in vitro or in vivo maturation or fertilization. Three major classes of changes in total phosphoprotein synthesis are observed. In the first class, protein phosphorylations increase from the germinal vesicle stage until just after germinal vesicle breakdown and then decrease during progression to metaphase II and after fertilization. The second class is characterized by decreases in protein phosphorylation during maturation with subsequent increases in phosphorylation of these proteins after fertilization. The third class is characterized by protein phosphorylations that remain relatively constant during maturation but increase after fertilization; phosphotyrosine phosphoproteins comprise the major species. The radiolabeled protein and phosphoprotein composition of isolated germinal vesicles was also examined, and a phosphoprotein of Mr 29,000 is found exclusively associated with the germinal vesicle. Since we have shown previously that 12-O-tetradecanoyl phorbol 13-acetate inhibits fertilization (Y.Endo, R.M. Schultz, and G.S. Kopf, submitted), we examined the effects of this compound on the phosphoprotein patterns of metaphase II eggs. 12-O-Tetradecanoyl phorbol 13-acetate treatment stimulates the phosphorylation of a specific phosphoprotein of Mr 80,000.

1-Methyl-3-isobutylxanthine↗
PubMed2000

Surface expression and rapid internalization of macrosialin (mouse CD68) on elicited mouse peritoneal macrophages.

Macrosialin, the mouse homolog of human CD68, is a heavily glycosylated transmembrane protein found almost exclusively in macrophages. Its function remains uncertain. It has a high affinity for oxidized low-density lipoprotein (LDL) in ligand blots and antibodies against the human homolog, CD68, inhibit the binding of oxidized LDL to a human monocyte-derived cell line (THP-1). However, there is still controversy as to whether macrosialin, found predominantly in late endosomes, is expressed at all on the plasma membrane. The present studies, done in thioglycollate-elicited peritoneal macrophages, confirm that macrosialin is predominantly intracellular but show clearly that 10-15% of it is expressed on the cell surface. Exchange with intracellular pools occurs at an extremely high rate. The results are compatible with a surface function, including internalization of bound ligands or adhesion to surfaces.

Animals↗
PubMed2003

Synergistic antiviral effect of a combination of mouse interferon-alpha and interferon-gamma on mouse hepatitis virus.

Although interferon (IFN)-alpha and IFN-gamma have been reported to exhibit a synergistic antiviral effect through the different signaling pathways in vitro, their therapeutic efficacy is not well defined in vivo. The current study was carried out to investigate the combined antiviral effect in a model of mouse hepatitis virus Type 2 (MHV-2) infection, in which fulminant hepatitis is developed. MHV-2 was injected intraperitoneally into 4-week-old ICR mice, IFN or the vehicle was administered intramuscularly for 5 days, and the antiviral effect was evaluated based on survival periods, liver histology, serum alanine transaminase (ALT) levels, and MHV-2 virus titers in the liver tissues. The animals in the group treated with a combination of IFN-alpha and IFN-gamma survived for longer periods than the groups treated with IFN-alpha alone and IFN-gamma alone (IFN-alpha 10(3) (IU/mouse)/-gamma 10(3) vs. IFN-alpha 10(3), P < 0.005; IFN-alpha 10(3)/-gamma 10(3) vs. IFN-gamma 10(3), P < 0.001). This is consistent with the lower levels of hepatocellular necrosis and serum ALT and the decreased titers of MHV-2 virus in the liver tissues (48 hr, P < 0.001; 72 hr, P < 0.001). These findings indicate that a combination of IFN-alpha and IFN-gamma exhibits a synergistic antiviral effect on MHV-2 infection. The biology of MHV-2 is quite different from that of human hepatitis viruses; however, these results suggest the beneficial combined therapy of IFN-alpha and IFN-gamma for the treatment of human viral hepatitis.

Animals↗
PubMed2005

Pharmacodynamic interactions between recombinant mouse interleukin-10 and prednisolone using a mouse endotoxemia model.

The pharmacodynamic interactions between recombinant mouse interleukin-10 (IL-10) and prednisolone were examined in lipopolysaccharide (LPS)-induced experimental endotoxemia in Balb/c mice. Treatment phases consists of single doses of IL-10 (10 microg/kg i.p.), prednisolone (25 (mg/kg i.p.), IL-10 (2.5 microg/kg i.p.) with prednisolone (6.25 mg/kg i.p.), or placebo (saline). Measurements included plasma steroid kinetics and IL-10 concentrations and responses to LPS including proinflammatory cytokines (TNF-alpha, IFN-gamma) and circulatory NO measured as plasma nitrate/nitrite concentrations. The intraperitoneal dosing of LPS produced large and transient elevations of plasma TNF-alpha, IFN-gamma, and NO concentrations. Noncompartmental and model fitting using extended indirect response models based on drug inhibition of multiphase stimulation of biomarkers by LPS were used to describe the in vivo pharmacodynamics and drug interactions. Dosing with prednisolone, IL-10, or their combinations produced strong inhibition of cytokine and NO production. The IC50 values of prednisolone ranged from 54 to 171 ng/mL, and IC50 values for IL-10 ranged from 0.06 to 0.69 ng/mL. The production of NO was described as a cascading consequence of the TNF-alpha and IFN-gamma plasma concentrations. The joint dosing of IL-10 with prednisolone produces moderately synergistic immunosuppressive effects in this system. Both drugs were sufficiently protective in suppressing the inflammatory mediators when administered prior to the LPS trigger, while such effects were modest when administered after the inflammatory stimulus was provoked. The integrated and complex pharmacokinetic/pharmacodynamic models well capture the in vivo processes, drug potencies, and interactions of IL-10 and prednisolone.

Animals↗
PubMed1981

Influence of mouse hepatitis virus on the growth of human melanoma in the peritoneal cavity of the athymic mouse.

Mouse hepatitis virus (MHV) infection was found in 15 of 40 athymic mice (Balb/c nu/nu) used in an experimental model designed to study the effect of cell mediated immunity on target human melanoma cells growing in the peritoneal cavity. Most non-MHV-infected mice died of peritoneal tumor within predictable periods following injection of the melanoma cells. Twelve of 15 MHV-infected mice which showed either poor or no tumor growth died of MHV infection, whereas only 3 showed good tumor growth. Peritoneal macrophages in the ascites from the MHV-infected mice were greatly reduced in number compared to those in the ascites from the non-MHV-infected mice. Although the fibrohistiocytic reaction was more prominent in the MHV-infected mice, other aspects of spleen and lymph node lymphocytic reactions exhibited no remarkable differences between the two groups. The possible mechanisms whereby MHV infection influences tumor growth in nude mice are discussed.

Animals↗
PubMed1987

Inhibition of in vitro fertilization by mouse anti-mouse sperm sera and preliminary antigen identification.

Antisperm antibodies are implicated as one causative factor of infertility, but the target antigens have not been identified. Immune responses to sperm antigens are qualitatively variable even within a single mouse strain. We took advantage of this variability and immunized individual female mice to allogeneic sperm to reflect their natural exposure during mating. We determined the ability of the individual sera to inhibit in vitro fertilization and to bind to sperm antigens separated by electrophoresis. Compared to preimmune sera, four of five immune sera significantly inhibited in vitro fertilization. The serum from individual mice bound variable panels of sperm antigens. By comparing the panels, we identified two polypeptides with molecular weights of 40,000 and 44,000 that were bound by all sera. We propose that these molecules may be good candidates for further investigation of the immunoprophylaxis of pregnancy.

Animals↗
PubMed1995

Molecular cloning of a mouse G-protein-activated K+ channel (mGIRK1) and distinct distributions of three GIRK (GIRK1, 2 and 3) mRNAs in mouse brain.

We cloned the mouse brain G-protein-activated K+ channel 1 (mGIRK1) cDNA and determined the complete nucleotide and amino acid sequences of the coding region. In in situ hybridization using specific oligonucleotide probes, the signals for the three mGIRK (mGIRK1, mGIRK2 and mGIRK3) mRNAs were shown to be distributed widely as well as differently in most brain regions except for the caudate-putamen. Further, at least one, usually several, mGIRK mRNA with variable combinations was observed in most brain regions. These findings suggested that mGIRK channels may be essential in most brain regions in a signal transduction mediated by various G-protein-coupled receptors and that different subunit organizations of the mGIRK channel might occur in different neurons, resulting in diversity of their channel function in vivo.

Amino Acid Sequence↗
PubMed1995

Developmental analysis of the Hba(th-J) mouse mutation: effects on mouse peri-implantation development and identification of two candidate genes.

The Hba(th-J) mouse mutation is a deletion on chromosome 11 that spans the alpha-globin complex and causes alpha-thalassemia in heterozygous animals and in utero death of embryos homozygous for the deletion. We hypothesised that one or more genes closely linked to the Hba locus are also deleted in these mutant mice and that deletion of these additional genes is responsible for the embryo lethality. We have analysed the developmental profile of mutant embryos using a PCR assay to distinguish homozygous embryos from wild-type and heterozygous embryos. No homozygous embryos are detectable on Day 6.5 of gestation and morphological analysis of embryos on Day 5.5 shows that both the embryonic and extraembryonic ectoderm of the egg cylinder are reduced in size and contain degenerate cells. Preimplantation homozygous embryos are morphologically normal with the same proportion developing to the blastocyst stage as control embryos. However, the cell number of homozygous embryos on Day 4.5 is significantly reduced due predominantly to a decrease in the cell number of the trophectoderm and not the inner cell mass. When homozygous blastocysts are plated in vitro, outgrowth of giant trophectoderm cells appears similar to that of wild-type embryos but outgrowth of the inner cell mass is affected. Cells from the inner cell mass of homozygous embryos appear to undergo necrosis and dissociate from the trophectoderm outgrowth after 3 to 4 days in culture. These studies demonstrate that the development of both the inner cell mass and the trophectoderm of embryos homozygous for the Hbath-J deletion is affected by the mutation. We have used quantitative Southern blotting to show that 3-methyladenine glycosylase (mpg) and dist1, two genes closely linked to the Hba locus on chromosome 11, are also deleted in this mutation. Reverse transcriptase-polymerase chain reaction analyses demonstrate that mpg and dist1 are normally expressed by preimplantation and early postimplantation embryos, whereas alpha-globin transcripts from the Hba locus are not detected until Day 7.5 of gestation. These studies demonstrate that deletion of the mpg or dist1 genes is likely to be responsible for the homozygote embryo lethality and the potential roles of these gene products in early embryogenesis are discussed.

Animals↗
PubMed1997

Characterization of the binding of recombinant mouse sperm fertilin alpha subunit to mouse eggs: evidence for function as a cell adhesion molecule in sperm-egg binding.

Fertilin (previously known as PH-30) is a sperm protein that is a candidate molecule for mediating the binding and fusion of the sperm and egg plasma membranes. Fertilin is a heterodimer, with a beta subunit that has a region of homology to the disintegrin family of integrin ligands and an alpha subunit that has a region of homology to viral fusion peptides. It has been hypothesized that fertilin beta and alpha subunits mediate the interactions between sperm and egg plasma membranes, namely, binding and fusion, respectively. To address this hypothesis and to examine specifically the role of fertilin alpha in fertilization, we have expressed the predicted extracellular domain of mouse fertilin alpha as a bacterial fusion protein with maltose-binding protein. This fusion protein (hereafter referred to as recombinant fertilin alpha-EC) binds to the microvillar region of zona pellucida (ZP)-free eggs, the region of the membrane to which sperm bind. This binding is reduced in the absence of divalent cations and is supported by Ca2+, Mg2+, or Mn2+. Eggs that have been treated with chymotrypsin bind less recombinant fertilin alpha-EC than do untreated eggs, suggesting that a chymotrypsin-sensitive binding site for recombinant fertilin alpha-EC is present on egg surfaces. Binding to eggs is also affected by the method used to remove the ZP. Finally, recombinant fertilin alpha-EC inhibits the binding of sperm to eggs during in vitro fertilization of ZP-free eggs. These data are the first evidence to suggest that fertilin alpha can function as a cell adhesion molecule during fertilization, mediating the binding of sperm and egg plasma membranes.

ADAM Proteins↗
PubMed1995

Expression of gamma-glutamyl transpeptidase in midgestation mouse yolk sac and mouse visceral yolk sac carcinoma cells.

gamma-Glutamyl transpeptidase (gamma GT) is a crucial enzyme for the metabolism of xenobiotics and endogenous mediators of biological functions (leukotrienes, prostaglandins, and hepoxillins). Yet little is known about its potential role during development. It is a single copy gene expressed from at least seven promoters. Using histochemistry and immunohistochemistry we demonstrate that gamma GT first appears in the midgestational yolk sacs of mouse embryos. Established cell lines with phenotypic features of yolk sac endoderm (JC-44) or embryonic stem cells were also assayed for the expression of gamma GT. Significant levels were detected in JC-44 cells and higher levels were found in JC-44-derived embryoid bodies. Because this cell line appears to be a good in vitro counterpart of yolk sac differentiation, we characterized the gamma GT mRNA types expressed in JC-44 cells. By ribonuclease protection analysis, gamma GT RNA types IV and VI represent about 80% of the total gamma GT RNA in JC-44 embryoid bodies. Reverse transcription-mediated polymerase chain reaction detected low amounts of gamma GT RNA types I, III, and V. Expression of gamma GT in yolk sac follows a pattern seen in many tissues in which one or two gamma GT RNA types dominate the expression profile; however, the reason for this tissue specificity is unknown.

Animals↗
PubMed2000

Involvement of platelets in experimental mouse trypanosomiasis: evidence of mouse platelet cytotoxicity against Trypanosoma equiperdum.

Platelets play an important role in the human response to parasites. Trypanosoma equiperdum, a parasite that has the horse as its natural host, is able to induce infection in mice and thus it may represent a simple model for studying the role of platelets in the development of a parasitosis. Although several aspects of the murine response to T. equiperdum infection have been clarified, the precise mechanism of killing of the parasite is still unclear. We have studied the involvement of blood platelets in experimental murine infection with T. equiperdum. Infected mice show a progressive decrease of the number of circulating platelets. The production of thromboxane A2 (TxA2) by platelets stimulated with collagen decreases progressively with the progression of T. equiperdum infection, compatible with in vivo platelet activation or with a possible antagonistic effect by trypanosomes on the production of TxA2. Finally, mouse platelets exert in vitro a direct parasitocidal activity on T. equiperdum at ratios >/=20:1. Complement fractions do not enhance platelet trypanocidal activity, whereas IgM fractions do, at least in short-term coincubation experiments. Our data show that platelets are involved in experimental murine T. equiperdum infection and confirm that platelet parasitocidal activity is a generalized phenomenon in mammals.

Analysis of Variance↗
PubMed2001

Structure of the mouse Stat 3/5 locus: evolution from Drosophila to zebrafish to mouse.

Signal transducers and activators of transcription (Stat) are transcription factors that can be activated by many cytokines. While Drosophila contains only one Stat (d-Stat), mammals contain seven, with STATs 3, 5a, and 5b being the closest functional relatives. To understand the evolutionary relationship between d-Stat and vertebrate STATs 3 and 5, we isolated, sequenced, and analyzed the zebrafish Stat3 (z-Stat3) gene and a 500-kb region spanning mouse chromosome 11, 60.5 cM containing three Stat genes (m-Stats). Within this region we identified the genes encoding m-Stats 3, 5a, and 5b, Cnp1, Hcrt/Orexin, Ptrf, GCN5, mDj11, and four new genes. The 5' ends of the m-Stat5a and m-Stat5b genes are juxtaposed to each other, and the 3' ends of the m-Stat3 and Stat5a genes face each other. While the m-Stat5a and m-Stat3 genes have one promoter each, which are active in many tissues, the m-Stat5b gene acquired two distinct promoters. The distal promoter is expressed ubiquitously, and transcription from the proximal promoter is restricted to liver, muscle, and mammary tissue. Through a comparison of exon-intron boundaries from the m-Stat3, m-Stat5a, and m-Stat5b, z-Stat3, and d-Stat genes, we deduced their evolutionary relationship. We propose that the Stat3 and Stat5 lineages are derived from the duplication of a common primordial gene and that d-Stat is a part of the Stat5 lineage.

Animals↗
PubMed1999

Targeted disruption of the Cln3 gene provides a mouse model for Batten disease. The Batten Mouse Model Consortium [corrected].

Batten disease, a degenerative neurological disorder with juvenile onset, is the most common form of the neuronal ceroid lipofuscinoses. Mutations in the CLN3 gene cause Batten disease. To facilitate studies of Batten disease pathogenesis and treatment, a murine model was created by targeted disruption of the Cln3 gene. Mice homozygous for the disrupted Cln3 allele had a neuronal storage disorder resembling that seen in Batten disease patients: there was widespread and progressive intracellular accumulation of autofluorescent material that by EM displayed a multilamellar rectilinear/fingerprint appearance. Inclusions contained subunit c of mitochondrial ATP synthase. Mutant animals also showed neuropathological abnormalities with loss of certain cortical interneurons and hypertrophy of many interneuron populations in the hippocampus. Finally, as is true in Batten disease patients, there was increased activity in the brain of the lysosomal protease Cln2/TPP-1. Our findings are evidence that the Cln3-deficient mouse provides a valuable model for studying Batten disease.

Animals↗
PubMed1993

The detection and characterization of multiple hemagglutinin-esterase (HE)-defective viruses in the mouse brain during subacute demyelination induced by mouse hepatitis virus.

It has previously been shown that passive immunization with antibodies specific for the hemagglutinin-esterase (HE) protein of mouse hepatitis virus (MHV) prevents acute lethal encephalitis, resulting in a subacute and chronic demyelination in mice infected with JHM(2), an isolate of the neurotropic JHM strain of MHV. To determine possible genetic changes occurring during infection, viruses were isolated from the brain of infected mice at various time points after infection and examined for the patterns of their structural proteins. The results showed that the sizes and expression levels of the viral spike, membrane, and nucleocapsid proteins were constant among 161 virus isolates throughout the infection. In contrast, most of the viruses isolated later in infection did not synthesize HE protein. This finding suggests that the HE gene expression is extremely variable and is preferentially lost during prolonged viral infections. In contrast, when viruses were passaged in tissue culture, no significant accumulation of HE protein-defective mutants was observed, suggesting that the accumulation of HE protein-defective mutants in infected animals was most likely the result of the positive selection for these mutants during the subacute and chronic infection. The genetic defects of HE gene in these mutants were characterized by cloning, sequencing, and in vitro translation of HE genes. Most of the mutations in the HE protein-defective mutants consisted of deletions of various lengths at different sites within the HE-coding region, resulting in the change of the reading frame and early termination. However, most of the truncated HE proteins were not detected in the infected cells. Since viruses from different mice exhibited different types of defects, the HE mutations probably occurred de novo in the brain. These results demonstrated the exceptionally rapid selection of HE-defective mutants during viral infection of mice and suggest that their selection may be related to the neuropathogenicity or persistence of MHV.

Animals↗
PubMedDate not supplied

Inhibition of lung colonization of mouse colon 26 adenocarcinoma by recombinant mouse interferon beta through a modification of platelet function.

Recombinant murine interferon beta (MuIFN-beta) given i.v. efficiently inhibited both pulmonary arrest and formation of lung colonies of NL-17, a highly metastatic variant of mouse colon adenocarcinoma 26. NL-17 was rather resistant to MuIFN-beta in vitro and was highly resistant to natural killer cells of mice even though they were treated in vivo with MuIFN-beta. Platelets isolated from MuIFN-beta-treated mice showed reduced aggregating activity induced by NL-17. Since lung colonization by NL-17 is influenced by platelet aggregation, the inhibition of colonization by MuIFN-beta could be partly mediated through modification of platelet function in vivo. The effect of MuIFN-beta on platelet function and its subsequent inhibition of lung colony formation give new insights into the action of recombinant MuIFN-beta.

Adenocarcinoma↗
PubMed1981

A comparative scanning electron-microscopical study of endoneurial collagen around normal mouse nerve fibres, nerve fibres following crush injury and nerve fibres of the dystonic mouse mutant (dt/dt).

The endoneurial collagen sheath around teased nerve fibres following crush injury was studied by scanning electron microscopy and compared with uninjured sciatic nerve fibres and with fibres from the dystonic mutant mouse. Following crush injury the endoneurial collagen became more abundant than seen in untreated nerve fibres and formed large, seperate and longitudinally oriented bundles. However, by four weeks post injury the sheath regained a normal external appearance. Mutant nerve fibres were also associated with more than the usual amount of collagen, but the sheaths were more disorganised, with a marked disorientation and irregular aggregation of collagen, and these abnormalities were not confined to obviously degenerating or demyelinated regions of the fibres. The dystonic abnormalities of the endoneurial sheath may be important in the mechanism of the neuropathy.

Animals↗
PubMed1988

A rat model for imaging the effect of anti mouse antibody responses on the biodistribution of radiolabelled mouse monoclonal antibodies.

Rats were injected both intradermally and intravenously with an IgG2b mouse monoclonal antibody (791T/36) and subsequently the biodistribution of intravenously injected 111In labelled antibody was examined by gamma camera imaging in these and control rats. The majority of pretreated rats showed a marked perturbation of the biodistribution of the radiolabelled antibody with a marked increase of the tracer in the liver. There was similar perturbation of the biodistribution of subsequently administered 111In labelled Fab fragment of the 791T/36 antibody and of another IgG2b monoclonal antibody. In contrast, there was little influence on the biodistribution of IgG2a or IgG1 monoclonal antibodies, indicating that the response in the rats was predominantly against the IgG2b isotype. This rat model system is amenable to examination of a number of aspects of the biological consequences of immune responses to foreign immunoglobulins relevant to their use for clinical imaging.

Animals↗