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At least 361 records · Page 20Linked to original sources
PubMed1994

Lack of expression of the tryptase mouse mast cell protease 7 in mast cells of the C57BL/6J mouse.

Although the steady-state level of the mouse mast cell protease (mMCP) 7 transcript is below detection in the serosal and mucosal mast cells of the BALB/cJ mouse, the IL-3-dependent, bone marrow-derived mast cells (mBMMC) of this strain and four other strains contain a high steady-state level of the mMCP-7 transcript. To further analyze the expression of this mast cell tryptase, a mMCP-7-specific IgG was obtained by immunizing a rabbit with a 19-residue synthetic peptide that corresponds to its unique amino acid sequence at residues 160 to 178 (anti-mMCP-7(160-178). In a SDS-PAGE/immunoblot analysis of lysates of BALB/cJ mBMMC, anti-mMCP-7(160-178) IgG recognized a diffuse 31- to 36-kDa protein, which shifted to a sharp 27-kDa protein after treatment with N-glycanase. As assessed immunohistochemically, mMCP-7 protein is present not only in the secretory granules of BALB/cJ mBMMC, but also in the ear mast cells of this strain. In contrast, the ear mast cells of the C57BL/6J mouse do not contain detectable levels of mMCP-7 protein, although the ear mast cells of both mouse strains contain mMCP-5 protein. Because mMCP-7 mRNA and protein also were not detected in mBMMC from the C57BL/6J mouse, the failure of the ear mast cells of this strain to express mMCP-7 is most likely a consequence of an intrinsic abnormality in the mast cell-committed progenitor cells themselves, or in the bone marrow microenvironment that induces its mast cell progenitor cells to express this tryptase.

Amino Acid Sequence↗
PubMed1993

Interleukin-1 dose, mouse strain, and end point as they affect protection of mouse jejunum.

Interleukin 1 (IL-1) has been shown to protect a number of normal tissues against radiation injury. In mouse jejunum, modest protection against radiation injury has been reported using only the in vivo crypt survival assay in one mouse strain. The major goal of this study was to determine the protective effect of IL-1 on mouse jejunum using two assays of damage, crypt cell survival and lethality from radiation-induced crypt cell depletion, in two mouse strains, C3Hf/Kam and BALB/c nu/+, which were bred and maintained in a specific-pathogen-free barrier colony. In addition, the dependence of protection on the IL-1 dose in both assays was determined. Our findings showed that IL-1 protection of crypt cell depletion and subsequent death of the animals from loss of these cells was dependent on the IL-1 dose. We found that the amount of protection by IL-1 was related to the criterion used to assess the protection. For example, if protection was determined as a ratio of D10's or LD50/10, a bigger DMF was obtained for BALB/c mice than C3H mice with the same IL-1 dose, suggesting that C3H mice were not as well protected. However, if protection was determined by the increase in crypt cell number after IL-1, there was an identical 2.4-fold increase in crypt cells after the same IL-1 dose in both strains. On the basis of this criterion, then, protection of crypt cells by IL-1 did not depend on the mouse strain. Although the effect of IL-1 on animal survival at 10 days was strain dependent, the difference was related to differences in the slopes of the respective crypt cell survival curves for the two strains and not to different effects of IL-1 in the two strains tested.

Abdomen↗
PubMed1993

Glycosylation of human IgG subclass and mouse IgG2b heavy chains secreted by mouse J558L transfectoma cell lines as chimeric antibodies.

Oligosaccharide profiles for monoclonal chimeric mouse-human and mouse IgG2b antibodies produced in the mouse J558L cell line have been determined. These chimeric antibodies share the same mouse light chain and VH region and have a single, complex, oligosaccharide moiety attached to residue 297 of the heavy chain. Since the panel of chimeric antibodies included each of the human IgG subclasses and a set of IgG3 proteins having single residue differences, it was possible to evaluate the contributions of the protein template, the cell line, and the culture conditions to glycosylation. The study shows that the J558L cell line glycosylates human heavy chains with oligosaccharides characteristic of mouse immunoglobulins. This includes a galactose alpha 1-->3 galactose structure not found in human IgG and for which most humans have naturally occurring "anti-Gal" antibodies. The extent of galactosylation was very dependent on the culture conditions and was maximal for still culture. The findings have significance for the production of antibodies for in vivo administration.

Animals↗
PubMed1993

Mouse interferon gamma pretreated hepatocytes conditioned media suppress cytochrome P-450 induction by TCDD in mouse hepatoma cells.

Mouse interferon gamma (IFN-G) markedly suppressed 7-ethoxyresorufin o-deethylase (EROD) activity when added at the same time as TCDD in mouse primary hepatocyte cultures. IFN-G, however, had no effect on EROD induction by TCDD in Hepa-1 cells, a mouse hepatoma cell line, or Hepa-1 cells cocultured with Kupffer cells when added directly to the culture. EROD induction by TCDD in Hepa-1 cells was suppressed when cells were cultured with IFN-G pretreated mouse hepatocytes conditioned media. The magnitude of suppression was related to the dose of IFN-G and the density of hepatocytes used for the preparation of the conditioned media. Treatment of the monoclonal antibody against IFN-G to the conditioned media did not block the suppression of EROD induction. The suppressive effect of IFN-G pretreated hepatocytes conditioned media on EROD induction, however, was blocked when the conditioned media was heated or treated with trypsin. These results suggested that IFN-G pretreated mouse hepatocytes may release a soluble protein factor(s) which suppressed the EROD induction by TCDD in Hepa-1 cells.

Animals↗
PubMed1995

Cloning of the mouse homologue of the deleted in colorectal cancer gene (mDCC) and its expression in the developing mouse embryo.

Loss of DCC gene expression has now been demonstrated in a wide variety of metastatic cancers. Here we present the nucleotide sequence and predicted amino acid sequence of mouse DCC. Mouse and human DCC share 96% identity at the amino acid level. Analysis of DCC mRNA expression throughout the mid and late stages of gestation in the mouse, demonstrated that DCC mRNA is expressed at significantly higher levels in the developing mouse embryo than in any adult tissue. In addition, we show that an embryo-specific, alternatively spliced, form of DCC is expressed in day 9.5 through day 18.5 embryos. The expression of both alternatively spliced forms of DCC is developmentally regulated such that the embryonic form of DCC predominates in day 9.5 and 10.5 embryos. In the later stage embryos the expression of this alternatively spliced form of DCC is down-regulated with respect to that of the adult form. Whole-mount in situ hybridization of day 11.5 mouse embryos revealed that DCC mRNA is expressed at high levels in the developing brain and the neural tube. However, no DCC mRNA could be detected in any other embryonic tissue at this stage of development. These observations suggest that during embryogenesis DCC may play a pivotal role in the development of the central nervous system.

Alternative Splicing↗
PubMedDate not supplied

The mouse Necdin gene is expressed from the paternal allele only and lies in the 7C region of the mouse chromosome 7, a region of conserved synteny to the human Prader-Willi syndrome region.

Prader-Willi syndrome (PWS) is a neurogenetic disorder resulting from the loss of paternal expression of gene(s) localized in the 15q11-q12 region. A new human gene encoding a putative protein with high homology to the mouse NECDIN protein has recently been characterized and mapped to chromosome 15q11-q12. It is expressed from the paternal allele only, suggesting its potential involvement in PWS. We now report the localization of the mouse Necdin gene in a region of conserved synteny to the human PWS region. We demonstrate the paternal specific expression of Necdin in the mouse central nervous system, and show that parental alleles display a differential methylation profile in the coding region. Finally, fluorescence in situ hybridization analysis reveals an asynchronous pattern of replication at the Necdin locus. These results clearly demonstrate imprinting of the mouse Necdin gene. Mouse models will be powerful tools in the study of human PWS phenotype and imprinting mechanisms.

Alleles↗
PubMed1976

A biochemical approach to the study of the transmission of mouse mammary tumor viruses in mouse strains RIII and C3H.

Mouse mammary tumor virus (MMTV) proviral sequences were detected in the cellular DNA of mammary tumors and livers of RIII and C3H mice by molecular hybridization with radioactively labelled MMTV 60-70S RNA or tritiated MMTV complementary DNA (cDNA). By means of DNA:DNA reassociation kinetics, the DNA of the mammary tumor cells of these two mouse strains were found to contain more MMTV proviral sequences than the DNA of liver cells of these same tumor-bearing mice. Evidence is also presented that the DNA of the liver cells lacks a part (approximately 25%) of the MMTV proviral sequences found in the mammary tumor cells of these mouse strains. The relationship of the extra MMTV proviral sequences found in mammary tumor cells to the early mammary tumor-igenesis seen in these mouse strains is discussed.

Animals↗
PubMed1995

Expression of the mouse mammary tumor virus long terminal repeat open reading frame promotes tumorigenic potential of hyperplastic mouse mammary epithelial cells.

The retrovirus mouse mammary tumor virus (MMTV) 3' long terminal repeat (LTR) contains an open reading frame (ORF) for a 36-kDa protein and encodes a superantigen activity [pORF(sag)]. We have tested the potential oncogenic activity of pORF(sag) in two immortalized mouse mammary epithelial cells. We subcloned MMTV LTR ORF DNA into the pRc/CMV mammalian expression vector in order to place LTR ORF transcription under the control of the constitutive CMV promoter. Mouse mammary epithelial cell lines TM3 and FSK7e4 were transfected and G418-resistant cell clones were isolated. Reverse transcription-polymerase chain reaction and Northern blot analyses revealed modest overexpression of LTR RNA in several transfected cell clones of each line. Individual cell clones were transplanted into cleared mammary gland fat pads of syngeneic BALB/c mice. The parental cell lines and FSK7e4-derived clones did not form tumors, whereas ORF-transfected clones derived from the TM3 cells formed tumors within 8 weeks in 100% of transplanted fat pads in multiple experiments. The tumor cells expressed exogenous LTR ORF RNA and were proven to be derivatives of TM3 cells based on a marker p53 mutation. Immunohistochemistry using a polyclonal antiserum raised against pORF(sag) expressed in insect cells revealed a cytoplasmic reaction in TM3-CMV-LTR tumor cells; a much weaker cytoplasmic reaction was detected in the transfected tissue culture cells. These observations suggest that MMTV pORF(sag) may act as an oncogene in certain mouse mammary epithelial cells and raise the possibility that pORF(sag) may have a role in mammary tumorigenesis. As the parental FSK7 cell line has produced only ductal outgrowths upon transplantation in vivo and the TM3 cell line produces a nontumorigenic hyperplasia, the results suggest further that pORF(sag) may influence the latter stages of mammary tumorigenesis, namely, the preneoplastic to neoplastic transformation.

Animals↗
PubMed1985

Dysdifferentiative nature of aging: age-dependent expression of mouse mammary tumor virus and casein genes in brain and liver tissues of the C57BL/6J mouse strain.

Many aspects of the aging process could be the result of cells slowly drifting away from their proper state of differentiation. This possibility has been studied by searching for an age-dependent increase in the expression of specific genes in tissues where expression of these genes would not normally be expected. In these studies, cDNA probes of specific genes are used in a DNA X NA hybridization assay to detect possible complementary RNA sequences in tissues of different-aged animals. Using this technique in past experiments, a qualitative increase in the RNA sequence complexity of mouse leukemia virus (MuLV) and a quantitative increase in the amount of alpha- and beta-globin RNA were found with increasing age in the brain and liver of the C57BL/6J mouse strain. We report here a similar age-dependent qualitative increase in the RNA sequence complexity for mouse mammary tumor virus (MMTV) but no quantitative or qualitative age-dependent change in casein RNA sequences for the same tissues and mouse strain.

Aging↗
PubMed1996

The mouse Wnt-10B gene isolated from helper T cells is widely expressed and a possible oncogene in BR6 mouse mammary tumorigenesis.

From libraries made from activated mouse T lymphocytes, we have isolated cDNAs encoding Wnt-10B, a new member of the Wnt family of developmental control genes. This protein appears to be the mammalian orthologue of Wnt-10B, first identified in several non-mammalian vertebrates and recently in mouse. The mRNA expression pattern of mouse Wnt-10B indicates that it is induced following activation of helper T cells, but is also expressed in a variety of other tissues and cells of fetal or adult origin. 93 bp at the 5' end of the cDNA clone are identical to sequences previously reported as 3' flanking genomic DNA adjacent to a mouse mammary tumor virus (MMTV) provirus in the MMTV-induced BR6 mammary tumor, W26. Sequence analysis of tumor-derived genomic DNA confirms that the entire Wnt-10B gene is immediately adjacent to the provirus, suggesting that MMTV integration drives transcription of Wnt-10B, possibly contributing to the oncogenic process. Consistent with this idea is the detection of hybrid MMTV-Wnt-10B transcripts in BR6 tumor cells. T cells which produce abundant Wnt-10B mRNA were also found to produce protein.

Amino Acid Sequence↗
PubMed1984

Mouse mammary tumor virus: specific methylation patterns of proviral DNA in normal mouse tissues.

The methylation state of endogenous mouse mammary tumor virus (MuMTV) proviral DNA was examined in normal mouse tissues. DNAs from various tissues were cleaved with the methylation-sensitive enzymes HhaI and HpaII and analyzed by Southern blotting. Tissue-specific MuMTV proviral DNA methylation patterns were found in the BALB/c, C3H, C57BL, GR/A, and GR-Mtv-2- mouse strains. MuMTV proviral DNA was hypomethylated in DNAs from the spleens and testes of all strains examined. The GR/A mouse strain, which was most thoroughly studied, also showed hypomethylation of MuMTV proviral DNA in bone marrow and placental tissues. Analysis of RNAs extracted from GR/A liver, mammary tumor, testes, placenta, and spleen tissues demonstrated that MuMTV proviral hypomethylation need not reflect significant proviral transcription.

Cell Transformation, Viral↗
PubMed1986

Transfer, by selective breeding, of the pathogenic Mtv-2 endogenous provirus from the GR strain to a wild mouse line free of endogenous and exogenous mouse mammary tumor virus.

The GR laboratory mouse strain has five endogenous proviral copies of the mouse mammary tumor virus (MMTV). One of these, Mtv-2, is unique because it causes mammary carcinomas in virtually 100% of breeding GR females prior to 1 year of age. To facilitate studies of this locus in particular, and mammary tumorigenesis in general, we genetically tailored a new mouse line, WXG-2, which bears Mtv-2 as its only endogenous MMTV provirus. The WXG-2 line was constructed by making hybrids between the GR strain and a wild mouse line free of both endogenous and exogenous MMTV, backcrossing to the MMTV-free line, and fixing the Mtv-2 locus in a population with the desired genotype. Mammary tumors were observed in 5 of the 20 hybrid females carrying the endogenous Mtv-2 provirus. The WXG-2 line represents a new model system for studying MMTV-induced mammary tumorigenesis in the absence of multiple endogenous proviruses.

Animals↗
PubMed1987

A new common integration region (int-3) for mouse mammary tumor virus on mouse chromosome 17.

Mus musculus subsp. musculus (Czech II) mammary tumor DNA frequently contains an integrated proviral genome of the mouse mammary tumor virus (MMTV) within a specific 0.5-kilobase-pair region of the cellular genome (designated int-3). Viral integration at this site results in activation of expression of an adjacent cellular gene. We mapped int-3 to mouse chromosome 17 by analysis of PstI-restricted cellular DNAs from mouse-hamster somatic cell hybrids. Restriction analysis of cellular DNA from (C3H/OuJ X Czech II) X Czech II backcross mice established the gene order T-H-2-int-3. These results demonstrated that the int-3 locus is distinct from two other common integration regions for mouse mammary tumor virus (designated int-1 and int-2) in mammary tumor DNA and suggest that several cellular genes may be at risk for virally induced activation during mammary tumor development.

Animals↗
PubMed1991

Host genetic background effect on the frequency of mouse mammary tumor virus-induced rearrangements of the int-1 and int-2 loci in mouse mammary tumors.

The frequency with which int-1 and int-2 are rearranged in mouse mammary tumors by mouse mammary tumor virus (MMTV)-induced insertional mutagenesis is a consequence of the host genetic background. In 75% of C3H mammary tumors, int-1 is rearranged by MMTV insertion, whereas only 30% of BALB/cfC3H tumors contain a virus-induced rearrangement of int-1. This difference is significant (P less than 0.005) and could not be accounted for by the potentially additive effect of the genetically transmitted Mtv-1-encoded virus in C3H mice. Similarly, MMTV-induced rearrangement of the int-2 gene in mammary tumors of the R111 mouse strain (59%) occurred at a significantly (P less than 0.025) higher frequency than in BALB/cfR111 (25%) mammary tumors. Moreover, in BALB/cfR111 mammary tumors, there is evidence that rearrangement of int-1 and int-2 does not occur independently (P less than 0.025). These results suggest that the long history of inbreeding for high tumor incidence of C3H and R111 mouse strains has selected for the fixation of host mutations which either complement the action of the particular int gene or affect the sensitivity of specific subpopulations of mammary epithelium to infection by particular strains of MMTV.

Animals↗
PubMed1984

Mouse mammary tumor virus integration regions int-1 and int-2 map on different mouse chromosomes.

Two regions of mouse DNA which constitute common provirus integration sites in tumors induced by mouse mammary tumor virus have been identified and designated int-1 and int-2. By examining a series of hamster-mouse somatic cell hybrids, we mapped the int-2 locus to mouse chromosome 7 and confirmed the previous assignment of int-1 to chromosome 15. This constitutes proof that int-1 and int-2 are discrete genetic loci. It is therefore possible that proviral activation of two distinct cellular genes may result in the same neoplastic disease.

Animals↗
PubMed1984

Dexamethasone increases the number of RNA polymerase II molecules transcribing integrated mouse mammary tumor virus DNA and flanking mouse sequences.

In mouse Ltk- cells that were transfected with recombinant bacteriophage DNA containing a complete proviral copy of an integrated endogenous mouse mammary tumor virus (MMTV) with its flanking cellular sequences, the newly acquired MMTV proviruses were transcribed in a glucocorticoid-responsive fashion. After hormone treatment of selected cell clones in culture we isolated the nuclei, elongated the nascent RNA chains in vitro, and determined the number of RNA polymerase II molecules on the transcribed MMTV DNA as well as on the flanking mouse DNA sequences. We found that the specific increase in the polymerase loading after hormone treatment is proportional to the increase in the amount of stable MMTV mRNA. When the DNA sequences which are responsible for hormone-receptor binding and for the increased MMTV mRNA levels were deleted, no increase in RNA polymerase II loading on MMTV DNA was observed. Nuclear RNA chains which were transcribed in response to hormone treatment were detected not only from the transfected MMTV DNA but also from the mouse DNA sequences adjacent to the 3' end of the provirus.

Adenine Phosphoribosyltransferase↗
PubMed1986

High murine mammary tumor virus expression in milk in a low mammary tumor mouse strain and high incidence of mammary tumor in hybrids produced by crossing with another low mammary tumor mouse strain.

Large amounts of murine mammary tumor virus (MMTV) were expressed in milk from a low mammary tumor mouse strain called II-TES, established by crossbreeding DBA/2 mouse strain with two strains of Japanese pet mouse origin. The reciprocal hybrids of the II-TES strain and OZ-F strain, another low mammary tumor strain of Japanese pet mouse origin, developed early-appearing mammary tumors at a high rate, and large quantities of MMTV were expressed in the milk. These findings suggest that different regulatory genes control MMTV expression and mammary tumorigenesis.

Animals↗
PubMedDate not supplied

Hemizygous Tg.AC transgenic mouse as a potential alternative to the two-year mouse carcinogenicity bioassay: evaluation of husbandry and housing factors.

The dermal Tg.AC transgenic mouse model has been proposed as a potential alternative to the conventional (e.g. oral, dermal, parenteral, inhalation, etc.) 2-year rodent bioassay for detecting chemical carcinogenicity. The present study was designed to address a number of technical aspects of this model as well as to augment the database being developed with the Tg.AC system at the NIEHS. Hemizygous Tg.AC mice were implanted s.c. with microchips for identification and housed individually in polycarbonate (i.e. 'plastic') or suspended stainless-steel wire-bottom (i.e. 'metal') cages. Treatment consisted of dermal application of the test or control material in treatment volumes of 200 microl of acetone. Groups of 10 males and 10 females were treated as follows: G1--shaved, no treatment; G2--acetone control seven times a week; G3--100 microl of benzene three times a week; G4--150 microl of benzene three times a week; G5--1.25 microg of phorbol ester (PMA) twice a week. The G1-G5 mice were housed in plastic caging with Alpha-dri bedding. Three additional groups were housed in stainless-steel wire-bottom caging: G6--shaved, no treatment; G7--acetone control seven times a week; G8--1.25 microg of PMA twice a week. The PMA-treated mice (G5 and G8) served as the positive controls. Mice were treated for 20 weeks followed by a 6-week recovery period prior to necropsy. The incidence of dermal papillomas in the shaved area was recorded weekly. There were no spontaneous papillomas in the target area of any of the untreated (G1) or vehicle control (G2) animals in the polycarbonate cages. One papilloma was observed in the untreated mice (G6) and one in the vehicle control group (G7) in the steel cages. This suggests that the type of caging, the shaving process, microchip implantation and daily acetone treatment for 20 weeks are all consistent with a very low background incidence of papillomas in this model. Papillomas were observed in the positive control groups as early as 4 weeks of treatment and increased both in number per mouse and number of mice affected up to a maximum average of 3.5 papillomas per mouse and 55% (11/20) mice with papillomas in G5 and 2.7 and 80% (16/20) in G8. A plateau was reached at about week 13 and the numbers of papillomas remained stable through the rest of the treatment and recovery phases. The low dose of benzene (100 microl) showed no significant effect, whereas the higher dose (150 microl) produced a moderate number of papillomas beginning at about week 11. The results of this study are comparable with earlier studies at the NIEHS and indicate reproducibility between laboratories and that the Tg.AC transgenic mouse model is suitable for use in an industrial pre-clinical safety evaluation context.

Acetone↗