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At least 721 records · Page 40Linked to original sources
PubMed1984

Mouse erythrocyte membrane sialoglycoproteins and their involvement in the interaction with mouse rosette forming human lymphocytes.

Sialoglycoproteins were isolated from Balb/c mouse erythrocyte membranes. The crude preparation showed four PAS-positive zones in SDS-polyacrylamide gel electrophoresis. The lowest molecular weight component was separated on the Ultrogel AcA44 column in the presence of SDS. The carbohydrate composition of the fractions obtained indicated that the sialoglycoproteins contained O-glycosidic oligosaccharide chains and and that the lowest molecular weight glycoprotein also contained N-glycosidic chain(s). The sialoglycoproteins strongly and specifically inhibited the rosette formation between mouse erythrocytes and human B lymphocytes. It suggested that sialoglycoproteins were the mouse red cell components involved in the interaction with human lymphocytes.

Animals↗
PubMed1977

The influence of antisera specific for alpha-fetoprotein and mouse serum albumin on the viability and protein synthesis of cultured mouse hepatoma cells.

The cytotoxic potential of heterologous rabbit antibody directed against mouse serum albumin (MSA) and alpha-fetoprotein (AFP) was investigated in vitro with a cell line (Hepa) derived from the mouse hepatoma BW7756. Anti-AFP in the presence of complement could kill Hepa cells at concentrations of anti-MSA that were virtually nontoxic. The specificity of the anti-AFP was defined by demonstrating that Hepa cell toxicity was dependent upon and paralleled the secretion of AFP in synchronized cultures. Furthermore, neither antiserum could be shown to be significantly toxic to mouse neuroblastoma cells (Neuro-2A). Immunoglobulin purified from pools of antisera was also highly effective in producing cytotoxicity even in a complement-free system. This reaction proceeded more slowly, requiring nearly 48 hr to reach maximum effect in comparison to the 12 hr for complement-mediated toxicity. MSA and AFP are secreted during different phases of the cell cycle. In cultures arrested by isoleucine starvation, labeled AFP appears in the medium 10 hr after release of the blockade in association with S phase. The appearance of labeled MSA is delayed until the first mitosis. Cytotoxic effects of anti-AFP parallel the secretion of AFP in synchronous cultures. Both antisera could be inhibitory to the secretion and synthesis of the proteins of their antigenic specificity. MSA synthesis was more susceptible to this inhibition than was AFP synthesis. The significance of this phenomenon and its association with the differential cytotoxicity of the antiserum are discussed.

Antibodies↗
PubMed1981

Early mouse embryo intracisternal particle: Fourth type of retrovirus-like particle associated with the mouse.

Electron microscopy combined with a quantitative analysis was used to study the virus-like particles appearing in oocytes and preimplantation embryos of nine mouse strains: inbred AKR, NZB, BALB/c, and C3H/He; randomized Swiss; inbred DDK; noninbred Peru; and randombred Q and MF1. Main findings were as follows: 1) The omnipresence was noted in mice of a fourth type of retrovirus-like particle (referred to as epsilon-particle) clearly distinguishable from the known A-, B-, and C-type particles and resembling more closely the R-type particles of the hamster. 2) epsilon-Particles occur transiently within the endoplasmic reticulum of early cleavage-stage embryos and have not yet been observed in either oocytes or later embryos, in normal adult tissues, or in tumors. 3) Intracisternal A-particles, identical to those seen generally in mouse tumors, also occurred in oocytes and early embryos but by far in smaller numbers than did epsilon-particles. 4) The production of epsilon- and A-particles exhibited exactly inverse patterns of developmental stage dependence. These patterns were basically similar, regardless of the mouse strain examined. 5) In contrast, the mode of occurrence of C-type particles was subject to a great strain-dependent variation.

Age Factors↗
PubMed1982

Lymphocytes bearing Fc receptor for IgE. VIII. Affinity of mouse IgE for Fc epsilon R on Mouse B lymphocytes.

Fc epsilon R(+) lymphocytes were demonstrated in BALB/c, C57BL/6 and SJL strains of mice by a rosetting technique. The proportion of Fc epsilon R(+) lymphocytes in their spleens was 25 to 33% of the total cells. The majority of the Fc epsilon R(+) cells in the spleen of BALB/c mice were B cells, which also have Fc gamma R. However, after infection of mice with Nippostrongylus brasiliensis, a significant proportion of T cells also bore Fc epsilon R. The average number of Fc epsilon R per Fc epsilon R(+) cell in normal BALB/c spleens was 5100. These receptors were saturated with IGE after incubation of the cells with 5 micrograms/ml mouse IgE. The forward rate constant (k1) of the IgE binding to Fc epsilon R on normal B cells was 1.66 X 10(4) M-1 sec-1, while the dissociation rate of IgE from the Fc epsilon R was 1.7 x 10(-4) sec-1. The equilibrium constant between mouse IgE and Fc epsilon R on normal B cells was approximately 0.95 X 10(8)M-1. However, Fc epsilon R on mouse lymphocytes appeared to be heterogeneous with respect to their affinity for IgE. After infection of mice with Nippostrongylus brasiliensis, the number of Fc epsilon R per receptor-bearing lymphocyte increased several-fold. The FC epsilon R newly expressed after infection appeared to have a lower affinity for IgE than those present originally.

Animals↗
PubMed1995

Transformation of mouse cells by wild-type mouse c-Src.

Previous studies in which chicken and human c-Src were overexpressed in chicken and rodent cells have indicated that overexpression of wild-type c-Src can not induce complete neoplastic transformation. However, studies with v-Src mutants have demonstrated that species-specific differences can play a significant role in transforming activity. Here we show that, in contrast to chicken c-Src, overexpressed mouse c-Src can induce significant anchorage-independent growth and tumorigenicity when transfected into NIH3T3 mouse cells. The biochemical cause for this difference is unknown. In particular, the protein-tyrosine kinase activities of chicken and mouse c-Src appear to be similar. This result is consistent with the hypothesis that v-Src-induced transformation results from perturbation of signalling pathways modulated by c-Src and highlights the need for caution in controlling for potential species-specific differences in studies of c-Src function.

Animals↗
PubMed1995

Cis-acting DNA elements of mouse granulocyte-macrophage colony-stimulating factor gene responsive to Fc epsilon receptor cross-linking stimulation in the mouse mast cell line MC/9.

Mouse mast cells produce many kinds of cytokines in response to cross-linking of high affinity Fc epsilon receptor (Fc epsilon RI). Among these cytokines, granulocyte-macrophage CSF (GM-CSF) gene induction in mouse mast cells has been reported to be regulated at both the transcriptional level and the post-transcriptional level. We analyzed the mechanism of the transcriptional regulation of GM-CSF gene induction through Fc epsilon RI cross-linking stimulation in the mouse mast cell line MC/9. In MC/9, the GM-CSF gene was activated transcriptionally by Fc epsilon RI cross-linking stimulation. The 5' deletion analysis of GM-CSF gene promoter indicated that the 5' boundary of the responsive promoter region lay between positions -113 and -95. When the deletion was extended to positions -72 or -60, the stimulatory effect was significantly diminished. We then examined 3' deletion of pmGMCAT -113 from position -60. This analysis indicated that the 3' boundary lay between positions -84 and -72. No subfragments of the region spanning positions -113 to -72 could cover the full induction level. A site-directed mutagenesis experiment revealed that the sequence spanning positions -108 to -72 was needed for full activation. These data indicate that GM-CSF gene in mast cells is activated mainly through the sequence spanning positions -108 to -72.

Animals↗
PubMed1995

Production of mouse immunoglobulin G by a hybrid plant derived from tobacco-mouse cell fusions.

Mouse-tobacco hybrid calli, and complete plants producing mouse gamma-3 heavy and lambda light chains, have been generated by somatic cell fusions of mouse spleen cells and tobacco mesophyll protoplasts. Both gamma 3 and lambda chains were detected in hybrid calli and complete plants by enzyme-linked immunosorbent assay, immunofluorescent staining, and Western blotting. When cellular DNA from hybrid tobacco mesophyll protoplasts was amplified by the polymerase chain reaction (PCR) using two pairs of gamma 3 chain DNA primers and one pair of lambda chain DNA primers, the PCR products contained gamma 3 and lambda chain DNAs, which could be detected by southern blotting and DNA hybridization, using specific synthetic oligonucleotide probes for gamma 3 and lambda respectively. In situ hybridization of hybrid tobacco mesophyll protoplasts with specific recombinant DNA probes of gamma 3 and lambda chains showed the presence of gamma 3 and lambda chain DNAs in the hybrid protoplasts.

Animals↗
PubMed1993

Histochemical analysis of carbohydrate moieties and sugar-specific acceptors in the kidneys of the laboratory mouse and the golden spiny mouse (Acomys russatus).

The aims of this work were to histochemically compare the pattern of lectin binding and endolectin expression in different portions of nephrons of two rodent species producing either normal hyperosmotic urine (the laboratory mouse) or highly concentrated urine (Acomys russatus, the golden spiny mouse). A panel of biotinylated lectins and neoglycoproteins and the avidin-biotin-peroxidase complex technique were used on Bouin's fixed, paraffin-embedded sections. Various segments of the uriniferous tubule in both species showed differential affinity for labelled lectins and neoglycoproteins. Significant differences were also evident between comparable tubular segments in laboratory and golden spiny mouse kidneys. Whether the histochemical expression of sugar moieties of glycoconjugates as well as endolectins, thus both sides of presumed protein-carbohydrate interactions, may be correlated to the various glycoproteins which would include constituents of the glycocalyx and domains of a variety of transport enzymes deserves further studies.

Animals↗
PubMed1995

The SCID mouse reaction to human peripheral blood mononuclear leukocyte engraftment. Neutrophil recruitment induced expression of a wide spectrum of murine cytokines and mouse leukopoiesis, including thymic differentiation.

In this study, we describe the kinetics of host immune reactions occurring in mice with severe combined immunodeficiency (SCID) at different times after the intraperitoneal injection of human peripheral blood mononuclear leukocytes (huPBL). At 24 hr, a massive neutrophil recruitment and an induced expression of a wide spectrum of murine cytokine mRNA (i.e., interleukin [IL]-1 beta, IL-4, IL-6, IL-10, IL-12, tumor necrosis factor [TNF]-alpha and interferon [IFN]-gamma) occurred in the huPBL-SCID mouse peritoneal cavity. By using ELISAs specific for mouse cytokines, large amounts of IL-1-alpha, TNF-alpha, IL-6, and IFN-gamma were detected in the peritoneal washings of huPBL-SCID mice 1 day after intraperitoneal injection. IL-6 and IFN-gamma production persisted for up to 2 weeks after PBL transplantation. Medullary and extramedullary expansion of the SCID mouse hematopoietic cells also occurred in the chimeras as early as 1 week after injection, together with a marked thymic differentiation (murine CD4+/CD8+ cells) at 10-12 weeks after transplantation. On the whole, these results indicate that, after huPBL injection, SCID mice mount a complex multistage immune response. These host reactions should be taken into consideration for any accurate interpretation of results obtained using the huPBL-SCID model. The control of responses (by means of specific antibodies to murine cytokines and to granulocytes or through the use of anti-inflammatory drugs) may be helpful in improving the engraftment of huPBL in SCID mice and in furthering our knowledge of the T and B cell-independent natural immune reactions.

Animals↗
PubMed1997

Automated measurement of mouse apolipoprotein B: convenient screening tool for mouse models of atherosclerosis.

Although mice are commonly used for studies of atherosclerosis, investigators have had no convenient way to quantify apolipoprotein (apo) B, the major protein of atherogenic lipoproteins, in this model. We now report an automated immunoturbidimetric assay for mouse apo B with an NCCLS imprecision study CV < 5%. Added hemoglobin up to 50 g/L did not interfere with the assay, nor did one freeze-thaw cycle of serum samples. Assay linearity extends to apo B concentrations of 325 mg/L. We have used the assay to determine serum apo B concentrations under several atherogenic conditions, including the apo E "knock-out" genotype and treatment with a high-cholesterol diet. Our assay can be used to survey inbred mouse strains for variants in apo B concentrations or regulation. Moreover, the mouse can now be used as a convenient small-animal model to screen compounds that may lower apo B concentrations.

Animals↗
PubMed1998

Purification and characterization of heterologously expressed mouse CYP2A5 and CYP2G1: role in metabolic activation of acetaminophen and 2,6-dichlorobenzonitrile in mouse olfactory mucosal microsomes.

The metabolic activation of two known olfactory mucosal (OM) toxicants, acetaminophen (AP) and 2,6-dichlorobenzonitrile (DCBN), was examined with mouse liver and OM microsomes and purified, heterologously expressed mouse CYP2A5 and CYP2G1. In reconstituted systems, both isoforms were active in metabolizing DCBN and AP to metabolites that formed protein adducts. The formation of DCBN- or AP-protein adducts and other AP metabolites, including 3-hydroxy-AP and, in the presence of glutathione, AP-glutathione conjugate, was also detected in OM microsomal reactions and to a much greater extent than in liver microsomes. Evidence was obtained that CYP2A5 and CYP2G1 play major roles in mouse OM microsomal metabolic activation of DCBN and AP. Immunoblot analysis indicated that CYP2A5 and CYP2G1 are abundant P450 isoforms in OM microsomes. OM microsomal AP and DCBN metabolic activation was inhibited by 5- and 8-methoxsalen, which inhibit both CYP2A5 and CYP2G1, and by an inhibitory anti-CYP2A5 antibody that also inhibits CYP2G1. In addition, the roles of CYP1A2 and CYP2E1 in the OM bioactivation of AP and DCBN were ruled out by comparing activities of acetone-treated mice or Cyp1a2(-/-) mice with those of control mice. Thus, CYP2A5 and CYP2G1 may both contribute to the known OM-selective toxicity of AP and DCBN. Further analysis of the kinetics of AP and DCBN metabolism by the purified P450s suggested that CYP2A5 may play a greater role in OM microsomal metabolism of AP, whereas their relative roles in DCBN metabolism may be dose dependent, with CYP2G1 playing more important roles at low substrate concentrations.

Acetaminophen↗
PubMed1998

[Avoid the mouse-trap! Musculoskeletal injuries can be reduced by placing the mouse within shoulder space].

Somewhat more than 50 per cent of computer operators complain of problems in the neck, shoulders or arms. A possible source of such problems may be manipulation of the mouse. Women are more susceptible than men, possibly due to their smaller physical size and muscle power. With the mouse placed to the side of the keyboard, narrow-shouldered computer operators must lift their arm and turn it sharply outwards. It is preferable to place the mouse within the span of the shoulders and rest the entire forearm on the desk. A shorter keyboard might be the answer for narrow-shouldered people.

Computer Peripherals↗
PubMed1986

Glucocorticoid agonists as well as antagonists are effective inducers of mouse mammary tumor virus RNA in mouse mammary tumor cells treated with inhibitors of ADP-ribosylation.

Glucocorticoids increase expression of specific genes by a mechanism involving binding to and "activation" of a specific receptor protein. Other steroids, such as RU 486, bind to the glucocorticoid receptor but the resultant steroid-receptor complex is unable to activate glucocorticoid sensitive genes. In the present study we have observed that steroid regulation of the glucocorticoid-regulated mouse mammary tumor virus (MMTV) genome in cultured mouse mammary tumor cells is altered by treatment of the cells with inhibitors of (ADP-ribose)n synthetase. The ability of glucocorticoid agonists to increase MMTV is about 2-fold increased by the inhibitor treatment. Interestingly, RU 486 and other steroids that are normally inactive in control cells are very good inducers of MMTV in the treated cells. This alteration in MMTV expression is associated with a 37% increase in nuclear binding of the glucocorticoid, triamcinolone acetonide, and also RU 486 in the inhibitor-treated cells. Steroids that do not bind to the glucocorticoid receptor are not inducers in control or in treated cells. The results point to a role for ADP-ribosylation of proteins as a negative regulator of MMTV expression and suggest a mechanism for activation of steroid-sensitive genomes.

Adenosine Diphosphate↗
PubMed1998

Activation of Fgf8 in S115 mouse mammary tumor cells is associated with genomic integration of mouse mammary tumor virus.

Fgf8 is an embryonally expressed mitogenic fibroblast growth factor which has transforming capacity. It is expressed in S115 mouse mammary tumor cells (S115 cells) and in parental tumors of DD/Sio mice as well as in some human breast and prostate cancer cell lines. In S115 cells androgens induce the expression of Fgf8 which seems to be associated with the androgen-maintained malignant phenotype of the cells. S115 cells also contain and express Mtv proviruses known to insertionally activate oncogenes in other tumor cells. Here we studied the possibility of insertional activation of Fgf8 in S115 cells by MMTV proviral integration. We demonstrate by Southern blotting that the genomic DNA from DD/Sio tumors and S115 cells contains Mtv-sequences (Mtv-6 and Mtv-17) which are not found in the DNA from spleen or liver of the DD/Sio mice. In addition, the newly integrated Mtv-6 was localized to the DNA fragment containing the Fgf8 gene. Furthermore, the expression of Fgf8 mRNA in DD/Sio tumors and S115 cells was not found in mammary gland or spleen and liver of DD/Sio mice. In S115 cells, Fgf8 mRNA expression was induced in parallel to MMTV mRNA by androgen and glucocorticoids which supports the possibility that Fgf8 is controlled by the steroid-regulated MMTV-LTR. In conclusion, our data provide evidence that the insertion of MMTV into the DD/Sio tumor DNA is associated with the transcriptional activation of Fgf8 in DD/Sio tumor and consequently in S115 mouse mammary tumor cells.

Animals↗
PubMed1999

Antisense downregulation of a mouse mammary tumor virus activated protooncogene in mouse mammary tumor cells reverses the malignant phenotype.

Activation of the protooncogene Wnt-1 by insertion of the mouse mammary tumor virus (MMTV) is known to cause mammary tumors in mice. Wnt-1 expression in mammary glands has been postulated to confer direct local growth stimulation of mammary epithelial cells leading to their acquisition of a preneoplastic state. Wnt-1 expression also induces morphological alterations in cultured normal mammary cells. However, it has not been determined whether or not transformed mammary cells require continuous Wnt-1 expression for their ability to form tumors in vivo. To address this question, we constructed antisense and sense Wnt-1 expression vectors containing a synthetic promoter composed of five high-affinity glucocorticoid response elements (GRE5). This promoter is at least 50-fold more inducible by dexamethasone than the promoter contained in the long terminal repeats of MMTV. The vectors were introduced into a mouse mammary tumor cell line (R/Sa-MT) that expresses high levels of endogenous Wnt-1 mRNA and forms rapidly growing tumors when transplanted into syngeneic hosts. Of the 12 stably transfected cell lines established (9 with antisense and 3 with sense constructs), 2 antisense cell lines (R/Sa-MT/antisense) and 1 sense cell line (R/Sa-MT/sense) were examined for inducibility by dexamethasone of antisense and sense Wnt-1 RNAs, changes in endogenous Wnt-1 RNA expression, and changes in cell morphology. The growth patterns of the cells in vitro and in vivo were also examined. Our results show that (1) the levels of the expression of endogenous Wnt-1 mRNA and protein were reduced significantly (>80%) in those cells (R/Sa-MT/antisense) that expressed antisense Wnt-1 RNA at high levels following exposure to dexamethasone, compared to the R/Sa-MT/sense and R/Sa-MT control cells and (2) transplantation of the R/Sa-MT/antisense cells produced smaller tumors ( approximately 0.2 cm in 16 weeks) compared to the tumors ( approximately 2.0 cm in 8 weeks) that were produced by the R/Sa-MT/sense and R/Sa-MT cells. We therefore suggest that Wnt-1 expression is required not only for the transformation of normal mammary cells into tumor cells, but also for the maintenance of their tumorigenicity.

Animals↗
PubMed1981

Covert infection of a mouse mammary tumor cell line with Mycoplasma hyorhinis: cosedimentation with mouse mammary tumor virus in sucrose density gradients.

Supernatant fluids from cultures of a mouse mammary tumor (MT) cell line were found to produce a specific cell detachment effect when inoculated into HeLa cells. The cell detachment factor (CDG) responsible for this effect was examined. Repeated attempts to cultivate this CDF in bacteriologic, fungal, and mycoplasma media were unsuccessful. However, using the DNA fluorochrome staining technique and specific immunofluorescent staining procedures, the CDF was identified positively as a noncultivable strain of Mycoplasma hyorhinis. It was also noted that this CDF could be labeled with [3H]uridine in MT cell cultures, concentrated, and banded at a density of 1.18 g/cm3 when centrifuged to equilibrium in a 20 to 60% sucrose gradient. Using a multiple antibiotic treatment regimen, the MT cells were "cured" of the M. hyorhinis contaminant. Re-infection of these cells with an exogenous strain of M. hyorhinis resulted in the same cell detachment effect, and this strain when labeled with [3H]uridine also sedimented at a density of 1.18 g/cm3. The salient feature of these studies is that M. hyorhinis sediments at the same density of mouse mammary tumor virus (MMTV) in sucrose density gradients. This was demonstrated by sucrose density gradient analyses of a purified sample of MMTV, assaying for reverse transcriptase activity, and a [3H]uridine labeled sample of the M. hyorhinis present in the MT cell cultures.

Animals↗
PubMed1976

Propagation of mouse mammary tumor cell lines and production of mouse mammary tumor virus in a serum-free medium.

Five different mouse mammary tumor cell lines were propagated in a serum free medium. Evaluation of growth characteristics, including logarithmic growth, cell population increase, protein production and days to confluency, showed serum-free medium comparable to serum-containing medium. Mouse mammary tumor virus expression and production, in C3H and GR tumor cell lines, as determined by virus particle counting and RNA dependent DNA polymerase assays, subsequent to dexamethasone stimulation revealed equivalent to higher levels of virus in serum-free medium as compared to serum-containing medium.

Animals↗
PubMed1989

Caloric restriction perturbs the pituitary-ovarian axis and inhibits mouse mammary tumor virus production in a high-spontaneous-mammary-tumor-incidence mouse strain (C3H/SHN).

Dietary restriction (DR) retards aging and extends maximum life span. It is also known to decrease the incidence of hormone-dependent tumors. In the present investigation, we focussed primarily on the influence of DR on the pituitary-ovarian axis, and subsequently on gene expression of the mouse mammary tumor virus. F1 females from the mating of SHN female and C3H male mice were used in this study, since these hybrids display a very high incidence of mouse mammary tumors. The mice weaned at 3 weeks were raised on either a calorically-restricted diet (DR: 50 kcal/week; N = 5) or on a control diet (C: 95 kcal/week N = 5) for 5 weeks. Three C57BL/6J Jcl ad libitum-fed female mice, 8 weeks of age, were used as reference animals since this strain has a very low incidence of mammary tumors. The mean cellular contents of prolactin (PRL) and growth hormone (GH) in the pituitary, as determined by immunohistochemistry, were found to be reduced in mice raised on the DR diet. The decrease in the mean cellular content of PRL (50% of the mean control value) was accompanied by a decrease in the number of lactotrophs (17% of the mean value of control diet mice). However, the decrease in cellular content of GH (53% of the mean control value) was not accompanied by a decrease in the number of somatotrophs (no. of somatotrophs in DR = 103% of mean control value). Histologically, ovaries from DR mice showed many growing and atretic follicles, with few corpora lutea. In contrast, both control-diet and reference (C57BL/6J Jcl) mice showed two or three corpora lutea per ovarian section. In accordance with this finding, DR mice had not established stable estrus cycles by 8 weeks of age, in contrast to both control-diet and reference mice. Since caloric restriction has been shown to decrease mammary tumor virus (MMTV) gene expression, MMTV production was investigated by electron microscopy to confirm the validity of our experimental conditions. In DR or reference C57BL/6J Jcl mice, MMTV particles were rarely found in the mammary gland samples, but were always found in samples from control mice. The development of mammary glands, as indicated by the number of villi or the development of the rough endoplasmic reticulum, was delayed in DR mice. Thus, it was concluded that caloric restriction decreases the number of lactrotrophs, inhibits ovulation and delays mammary gland development. This immature status is considered to be due to perturbations in the pituitary-ovarian axis by caloric restriction.

Animals↗