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PubMed1993

Retinoic acid metabolites exhibit biological activity in human keratinocytes, mouse melanoma cells and hairless mouse skin in vivo.

Topical all-trans retinoic acid (RA) modulates growth and differentiation of skin and is used in the treatment of various dermatological disorders. RA is metabolized to 4-hydroxy RA, 4-oxo RA and 5,6-epoxy RA, which are believed to be markedly less active than RA. 3,4-didehydroretinoic acid (ddRA) is a metabolite of 3,4-didehydroretinol which is present in skin. ddRA is biologically active and acts as a morphogen. We have determined the relative biological activity of ddRA, 4-hydroxy RA, 4-oxo RA and 5,6-epoxy RA as assessed by three retinoid responsive systems relevant to skin. RA, ddRA, 4-hydroxy RA, 4-oxo RA and 5,6-epoxy RA (10-100 nM) reduced epidermal transglutaminase activity in human keratinocytes to similar extents, and inhibited alpha-melanocyte-stimulating hormone-isobutylmethylxanthine-inducible tyrosinase activity in Cloudman S-91 mouse melanoma cells by 67, 39, 48, 51 and 19%, respectively, at 100 nM. Daily topical application of the retinoids to hairless mouse skin for 4 days resulted in dose-dependent changes in epidermal thickness and global histological score. The relative potencies of RA, ddRA, 4-hydroxy RA, 4-oxo RA and 5,6-epoxy RA, as calculated by parallel line assay, were 1.0, 0.60, 0.34, 0.29 and 0.18, respectively, for epidermal hyperplasia and 1.0, 0.78, 0.23, 0.14 and 0.08, respectively, for global histological score. Interestingly, the compounds exhibited a similar rank order of potency with respect to induction of cellular retinoic acid binding protein-II mRNA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

[Histological analysis of spontaneous adenomyosis-like changes in recombinant inbred mouse uterus (SMXA mouse)--a novel animal model for adenomyosis].

The etiology and the pathogenesis of adenomyosis, which is a benign uterine disease featuring the ectopic proliferation of endometrial tissues and glands into the myometrium and the serosa in the uterus, are still unknown. A novel mouse strain, which showed signs of a condition resembling adenomyosis, was found and the localization of alpha-actin and tenascin was analyzed in order to characterize the histological features of this disease. 1. The uteri of recombinant inbred SMXA mice were shown to have undergone spontaneous histological changes similar to adenomyosis. 2. Compared with SMXA mice, the uteri of F1 mice between the SMXA and NJL strains showed further prominent changes resembling human adenomyosis, which suggests that some hereditary factors may be involved in the pathogenesis of adenomyosis. 3. In a normal mouse uterus, the regions in which tenascin was expressed change with the estrus cycle. In SMXA mice, tenascin was expressed around the dysplastic and cystic uterine glands, and in the myometrium. These results indicated that tenascin is an important marker of the histological changes in adenomyosis. 4. SMXA mice, which are recombinant inbred mice, are shown to be a useful animal model to use in analyzing the pathogenetic mechanisms of adenomyosis.

Animals↗
PubMed1994

Establishment of new SCID and nude mouse models of human B leukemia/lymphoma and effective therapy of the tumors with immunotoxin and monoclonal antibody: marked difference between the SCID and nude mouse models in the antitumor efficacy of monoclonal antibody.

BALL-1, a human B leukemia/lymphoma cell line, was transplanted into nude and SCID mice under various conditions. The transplantation was substantially improved by preadaptation of BALL-1 by serial passages in newborn and young nude mice. We were able to establish the desirable conditions where 100% of SCID and nude mice that were inoculated i.p. with various doses of the adapted BALL-1 (termed BALL-1a) developed tumors. Tumors in SCID mice were disseminated to various tissues in a manner analogous to tumors in patients with B leukemia/lymphoma, whereas tumors in nude mice were not as widely disseminated and grew mainly as ascites. Flow cytometric analyses showed that all of the 11 tested cell surface markers of the parental BALL-1 were well maintained on the tumor cells recovered from the SCID and nude mice. The utility of the developed tumor models for the therapeutic studies was investigated by i.p. or i.v. administration of an anti-B leukemia/lymphoma monoclonal antibody, termed SN7 (IgG1 kappa), and SN7 immunotoxin (IT) that was prepared by conjugating SN7 to ricin A chain (RA) or deglycosylated RA (dgRA). In the nude mouse model study, SN7-RA that had been administered i.p. suppressed the tumor growth completely in all of the treated mice (n = 5) without any sign of tumor or undesirable side effects for as long as followed (i.e., 350 days), whereas unconjugated SN7 showed only a slight therapeutic effect. A control RA conjugate was not effective. In the SCID mouse model studies, several sets of experiments were carried out by i.p. or i.v. administration of IT, monoclonal antibody, or control IT. In the first three sets of experiments, SCID mice inoculated with 1.1 x 10(6) BALL-1a cells received an i.p. administration of phosphate-buffered saline or three different doses (i.e., 4 x 10 micrograms, 4 x 20 micrograms, and 4 x 30 micrograms) of therapeutic agents (SN7-RA and SN7). Virtually an identical result was obtained from the three experiments. All of the phosphate-buffered saline control group mice (n = 15) died within 35 days post tumor inoculation. In contrast, all of the mice that were treated with SN7-RA (n = 19) or with SN7 (n = 15) survived for as long as followed (i.e., 250 days). However, the unconjugated SN7 was less effective than SN7 IT for tumor suppression in SCID mice that were inoculated with a larger tumor burden (i.e., 4 x 10(7) BALL-1a cells).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Polymorphism in the mouse Tap-1 gene. Association with abnormal CD8+ T cell development in the nonobese nondiabetic mouse.

Tap-1 and Tap-2 genes code for a heterodimeric peptide transporter required for the normal maturation and surface expression of class I molecules. Polymorphic variants of these MHC encoded genes occur in rats and humans. After failing to amplify a 3' polymerase chain reaction (PCR) product from thymic and splenic cDNA of the nonobese nondiabetic (NON) strain, we considered it possible that Tap-1 polymorphism was present, since cDNA from CBA/J, C57BL/6, BALB/c, and NOD (nonobese diabetic) mice all yielded Tap-1 3' products. Overlapping PCR fragments spanning the highly conserved ATP-binding cassette (ABC) were generated for purposes of restriction endonuclease analysis, studies of IFN-gamma regulation, and sequencing. To avoid amplifying other members of the transporter family, we used a gel-purified 1670-bp Tap-1 PCR "long product" as template for nested PCR. Sequencing revealed three polymorphic alleles. The most divergent was for the NON strain and involved two non-conserved amino acid substitutions (Arg-->Cys397 and Leu-->Arg491) and three silent mutations. NON mice show an abnormal pattern of class I (Kb) expression and a sizeable reduction in the percentage of CD8+ cells in the blood and thymus. In F2 segregants, the low CD8 phenotype mapped to the MHC. Tap-1 genes of NON and C57BL/6 mice were equally sensitive to up-regulation by IFN-gamma. We conclude that the mouse Tap-1 transporter gene, like the Tap-2 of the rat and the Tap-1 and Tap-2 of the human, is polymorphic. The extensive variation and specific codon changes of Tap-1 in the NON mouse raise the possibility that this gene is the MHC locus responsible for altering the intrathymic development of CD8+ T cells.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1993

Expression and functional properties of mouse B7/BB1 using a fusion protein between mouse CTLA4 and human gamma 1.

We report the construction and expression of a fusion protein made from the extracellular portion of the mouse CTLA-4 gene and the constant region of human IgG1. This fusion protein behaves like an antibody to mouse B7/BB1, binding to activated B cells and purified dendritic cells. In addition, we found it to bind to activated T cells. The fusion protein interfered with the ability of antigen-pulsed antigen-presenting cells to induce proliferation of T-cell clones, although the degree of inhibition varied. These findings are discussed in the light of the physiological activation of T cells in secondary lymphoid organs.

Abatacept↗
PubMed1993

Structure, chromosomal localization, and expression of mouse reg genes, reg I and reg II. A novel type of reg gene, reg II, exists in the mouse genome.

We previously identified a gene, reg (i.e. regenerating gene), in the screening of a regenerating islet-derived cDNA library of rat (Terazono, K., Yamamoto, H., Takasawa, S., Shiga, K., Yonemura, Y., Tochino, Y., and Okamoto, H. (1988) J. Biol. Chem. 263, 2111-2114), and isolated a human reg cDNA and gene (Watanabe, T., Yonekura, H., Terazono, K., Yamamoto, H., and Okamoto, H. (1990) J. Biol. Chem. 265, 7432-7439); the rat and human cDNAs encode 165- and 166-amino acid proteins, respectively. Until now, it was thought that there is a single locus for Reg protein in the mammalian genome. In this study, we isolated two distinct cDNAs and genes, one of which was a mouse homologue to rat and human reg gene, the other a novel type of reg gene. We designated them reg I and reg II, respectively. The two proteins encoded by these genes share 76% amino acid sequence identity with each other. Both genes span about 3 kilobase pairs, and the genomic organization of six exons and five introns is conserved between them. Chromosomal mapping studies indicate that the reg I gene is localized on mouse chromosome 12, whereas the reg II gene is localized on chromosome 3. By Northern blot analysis, both reg I and reg II mRNAs are detected in the normal pancreas and hyperplastic islets of aurothioglucose-treated mice, but not in the normal islets. It is remarkable that in the gallbladder reg I is expressed, but reg II is not.

Amino Acid Sequence↗
PubMed1996

Cultivation of mouse-mouse hybridomas producing IgM monoclonal antibodies.

The mouse-mouse hybridomas producing monoclonal antibodies (MAbs) for ABO blood group determination were cultivated for 10 days in 25 cm2 Roux bottles using standard cultivation medium (DMEM) with different foetal-calf serum (FCS) concentrations (2-13%). The highest specific production rates (200-1100 micrograms/10(6) cells/day) for MAbs were measured at the end of the cultivation: this phenomenon could be explained by advanced cell death and liberating the content of the cells into the medium.

ABO Blood-Group System↗
PubMed1996

Enhanced biological activity of human recombinant interleukin 2 coupled to mouse red blood cells as evaluated using the mouse Meth A sarcoma model.

In order to circumvent the toxicity associated with high-dose interleukin 2 (IL2) administration and its rapid clearance from the circulation, a carrier system for IL2 is needed. Red blood cells (RBCs) coated with recombinant interleukin 2 (rIL2) provide a means of delivering IL2 into the system in a continuous low-dose manner which, in turn, maintains a low, potentially non-toxic, IL2 concentration. Murine RBCs coated with rIL2 (RBCs-rIL2) are able to induce cytotoxic activity in mouse spleen cells in vitro against malignant murine YAC-1 cells (53-62% cytotoxicity) using less than 4500 i.u./10(9) RBCs per mouse. Cytotoxicity (21-31%) becomes apparent upon cytotoxic testing of spleens cells stimulated in vivo. Using the murine Meth A sarcoma model, the effectiveness of this RBC-rIL2 vehicle is demonstrated in vivo by a 84% reduction in tumour size as compared with the soluble-rIL2-treated mice. Moreover, the RBC-rIL2 vehicle is able to induce tumoricidal cytotoxicity with very low rIL2 concentrations (about 10,000 i.u. of rIL2/mouse). These results indicate that rIL2 retains its biological activity when bound to the RBC and therefore could prove useful as a therapeutic delivery system for cancer treatment.

Animals↗
PubMed1998

Transcription of a novel mouse semaphorin gene, M-semaH, correlates with the metastatic ability of mouse tumor cell lines.

In the attempt to identify genes associated with metastasis, we have compared gene expressions of two metastatic cell lines, 4T1 and 66cl4, and one noninvasive, nonmetastatic cell line, 67NR, which originate from the same mouse mammary adenocarcinoma. Using the technique of differential display, we identified a novel member of the semaphorin/collapsin family in the two metastatic cell lines. We have named it M-semaH. Northern hybridization to a panel of tumor cell lines revealed transcripts in 12 of 12 metastatic cell lines but in only 2 of 6 nonmetastatic cells and none in immortalized mouse fibroblasts. To our knowledge, this is the first time that the expression of a semaphorin gene has been shown to correlate positively with tumor progression. We have characterized two transcripts present in the tumor cells. One transcript, M-semaH-v, is a putative splice variant, which is less abundant in normal tissue and lacks 478 bp in the 3' untranslated region. Both transcripts encode the same 775 amino acids with the features of a secreted glycoprotein. Northern analysis suggests that the M-semaH gene is involved in embryonic development and in situ hybridization locates the M-semaH expression to the developing lungs, to developing skeletal elements, and to the ventral horns of the developing neural tube.

Amino Acid Sequence↗
PubMed1998

Altered expression of epidermal growth factor receptor ligands in tumor promoter-treated mouse epidermis and in primary mouse skin tumors induced by an initiation-promotion protocol.

Multiple epidermal growth factor receptor (EGFr) ligands have been identified, including transforming growth factor alpha (TGFalpha), heparin-binding epidermal growth factor (HB-EGF), amphiregulin (AR), and betacellulin (BTC). Previous work from our laboratory demonstrated that TGFalpha mRNA and protein are upregulated in epidermis during tumor-promoter treatment of mouse skin and in skin tumors produced by initiation-promotion regimens. The purpose of the study described here was to explore the role of other EGFr ligands in multistage skin carcinogenesis. A single topical treatment of either 12-O-tetradecanoylphorbol-13-acetate (TPA) or chrysarobin or a single full-thickness wound induced the expression of HB-EGF and AR in mRNA samples isolated from whole mouse skin. However, only full-thickness wounding significantly elevated expression of the BTC transcript. The levels of HB-EGF and AR transcripts were significantly elevated in skin tumors (both papillomas and squamous cell carcinomas) induced by initiation-promotion protocols. BTC transcript levels were low and barely detectable in all skin tumors examined. The level of keratinocyte growth factor (KGF) mRNA was also examined as a possible mechanism for upregulation of EGFr ligands. Only full-thickness wounding significantly elevated KGF transcript levels in whole-skin RNA samples. Furthermore, no evidence for upregulation of KGF mRNA in skin tumors was obtained. The results are discussed in terms of the role of EGFr activation in skin carcinogenesis and the mechanisms for altered regulation of EGFr ligands.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1998

Pig MHC mediates positive selection of mouse CD4+ T cells with a mouse MHC-restricted TCR in pig thymus grafts.

Remarkably normal immune function and specific T cell tolerance to discordant xenogeneic donors can be achieved by grafting fetal pig thymus and liver (FP THY/LIV) tissue to T cell and NK cell-depleted, thymectomized (ATX) mice. To determine whether or not host class II MHC molecules participate in the positive selection of mouse CD4+ T cells in FP THY/LIV grafts, we compared their development in ATX "AND" TCR-transgenic mice with positive selecting or nonselecting host MHC genotypes. Mouse TCR-transgenic CD4 single positive T cells repopulated the periphery significantly and to a similar extent in both T/NK cell-depleted, ATX AND mice with positive-selecting or nonselecting MHC backgrounds after grafting with FP THY/LIV. Therefore, MHC molecules from a widely disparate xenogeneic species can positively select T cells bearing a host class II MHC-restricted TCR without a contribution from the host MHC. These results, in combination with previous studies performed in this model, suggest that the T cell repertoire that is generated by the combination of positive selection on xenogeneic MHC and negative selection on both recipient and xenogeneic porcine MHC is tolerant of both donor and recipient and has sufficient cross-reactivity with host MHC/foreign peptide complexes to confer a high level of immunocompetence. The results have implications for the potential clinical applicability of xenogeneic thymic transplantation and also suggest a predominant role for the TCR recognition of species-conserved MHC residues in positive selection.

Animals↗
PubMed1980

Quantification of mouse mammary tumor virus structural proteins in hormone-induced mammary tumors of low mammary tumor mouse strains.

The expression of the mouse mammary tumor virus (MMTV) in hormone-induced mammary tumors was investigated by means of a radioimmunoassay for two major MMTV proteins, gp52 and p27. MMTV proteins were isolated on lectin affinity- and ion-exchange chromatography columns. The purified viral proteins were electrophoretically homogeneous and retained immunoreactivity after labelling with 125iodine. Standard competition assays showed that group-specific antigenic determinants were reacting. Mammary tumors were induced in three strains of mice with a low natural incidence of mammary tumors, C57BL, O20 and C3Hf, by a combined hormone treatment, consisting of hypophyseal isografts and administration of progesterone and estrone. Mammary tumors and mammary glands of hormone-treated animals were extracted and used for competition radioimmunoassays. In general, the tumorigenic hormone treatment resulted in enhanced amounts of MMTV proteins in the mammary glands, compared to the amounts found in lactating mammary glands of untreated animals. The levels of MMTV proteins in the mammary tumors were lower than in the mammary glands.

Animals↗
PubMed1986

Sequence, topography and protein coding potential of mouse int-2: a putative oncogene activated by mouse mammary tumour virus.

A major proportion of carcinomas induced by mouse mammary tumour virus (MMTV) show evidence for proviral activation of a cellular gene, int-2, on chromosome 7. The sequence of 7869 bp of DNA spanning the transcription unit of int-2 was determined and compared with that of a series of int-2-specific cDNA clones derived from mammary tumour RNA. The predicted positions of intron-exon boundaries, established by alignment of cDNA and chromosomal DNA sequences, indicate that the gene comprises at least three exons. An open reading frame capable of encoding a protein of 245 amino acids with an estimated mol. wt of 27 kd, is flanked by substantial non-coding segments at both 5' and 3' ends. Comparison of the chromosomal DNA sequence and the predicted amino acid sequence with available data-bases has revealed no homology to other known genes. These results are discussed in relation to the status of int-2 as a candidate proto-oncogene.

Amino Acid Sequence↗
PubMed1990

Demonstration of a new mouse mammary tumor virus locus in the genome of the mammary tumor prone strain SHN mouse.

Until this report, there have been no detailed analyses of the mouse mammary tumor virus (MMTV) loci in the mammary tumor prone strain SHN. Using a probe, which hybridizes to the env sequence of MMTV, Southern blotting of genomic DNA from the brain after digestion with EcoRI revealed 5 endogenous proviruses: Mtv-1 (4.5kb), Mtv-2 (11 kb), Mtv-8 (6.7kb), Mtv-17 (8.3kb) and a newly-found 6.5-kb fragment. F1-hybrid mice (C3H/He female x SHN male) also possessed the 6.5-kb fragment. Thus, we conclude that the 6.5-kb fragment is unique to SHN mice. Genomic DNA from mammary tumors of SHN mice showed MMTV insertions, suggesting that activation of an oncogene(s) occurred in this strain.

Animals↗
PubMed1979

Integration of the DNA of mouse mammary tumor virus in virus-infected normal and neoplastic tissue of the mouse.

We have used restriction endonucleases which cleave the DNA of mouse mammary tumor virus (MMTV) at one site (Eco RI) and several sites (Pst I, Sac I and Bam HI) to study infection and mammary tumorigenesis in mice. Proviruses acquired during infection of BALB/c mice foster-nursed by virus-producing C3H females can be distinguished from the MMTV proviruses endogenous to uninfected BALB/c mice by the nature of the fragments generated with Pst I and Bam HI. Using this assay, we show that lactating mammary glands as well as mammary tumors from BALB/cfC3H mice have acquired MMTV DNA, and that a minimum of approximately 10% of normal glandular cells can be infected. The new proviruses appear to be linked to cellular DNA of mammary tumors and infected lactating mammary glands within a limited region (0.2 x 10(6) daltons) of the viral DNA; the location of this region, based upon mapping studies with unintegrated MMTV DNA, suggests that the orientation of these proviruses is colinear with linear DNA synthesized in infected cells and thus approximately colinear with the viral RNA. Comparisons of many mammary tumors and studies of lactating mammary glands with a high proportion of independently infected cells indicate that a large number of sites in the cellular genome can accommodate a new provirus; the acquired proviruses are rarely, if ever, found in tandem with each other or with endogenous proviruses. We cannot, however, distinguish between random integration and integration into a large number of preferred sites in the host genome. Since Eco RI and Bam HI cleavage of DNA from each mammary tumor generates a unique set of viral-specific fragments, we propose that the tumors are composed principally of cells derived from a subset of the many infected cells in a mammary gland; this proposal is supported by our finding that Eco RI digestion of DNA from several transplants of a primary tumor yields the pattern characteristic of the primary tumor.

Animals↗
PubMed1981

Cloned mouse mammary tumor virus DNA is biologically active in transfected mouse cells and its expression is stimulated by glucocorticoid hormones.

We have cloned circular unintegrated mouse mammary tumor virus (MMTV) DNA from infected rat hepatoma cells in bacteriophage lambda. Seven independent clones containing MMTV DNA of homogeneous length of 9 kb (five) or 10 kb (two) were identified. The five 9 kb clones had identical restriction maps consistent with that of 9 kb unintegrated DNA; the other two were aberrant. MMTV DNA inserts were purified, ligated and used for cotransfection of Ltk- cells together with a plasmid containing the thymidine kinase gene of herpes simplex virus. All Tk+ cell clones acquired new MMTV sequences and those transfected with the 9 kb MMTV DNA synthesized normal viral RNA and proteins. Viral gene expression was increased by the addition of dexamethasone.

Animals↗
PubMed1987

Mammary preneoplasia and tumorigenesis in the BALB/c mouse: structure and modification of mouse mammary tumor virus DNA sequences.

Mouse mammary tumor virus (MMTV) DNA sequences were examined in mammary tissues from BALB/c mice, including both preneoplastic hyperplastic alveolar nodule (HAN) outgrowth lines, tumors derived from those preneoplastic tissues, and DMBA-induced mammary tumors. Over 60 different HAN and tumors samples were analyzed. The D2 HAN line contained one additional provirus, whereas Cv-2 and Cv-4 HAN lines that are infected with exogenous virus exhibited multiple virus integration events. D2 tumors showed the same provirus pattern as D2 HANs, whereas Cv-2 and Cv-4 tumors exhibited a subset of the acquired proviruses found in the parental HAN populations. Differential methylation patterns of virus-specific sequences were observed that resembled those described for other tissues in which viral DNA replication and integration has occurred, i.e., acquired proviruses were hypomethylated and endogenous proviruses were methylated. In tumors that arose from HAN lines and exhibited only endogenous proviruses, demethylation of the subgenomic Mtv-6 locus was observed. Demethylation of Mtv-6 was not detected in any of the preneoplastic tissues. Altered methylation of Mtv-8 and -9 was observed in both Cv-2 and Cv-4 tumors. Finally, mammary tumors induced by DMBA carried no acquired proviruses and demethylation of endogenous MMTV proviruses was demonstrated.

5-Methylcytosine↗
PubMed1979

Establishment of a C3Hf mammary tumor cell line expressing endogenous mouse mammary tumor virus: antigenic and genetic relationships of this virus with highly oncogenic mouse mammary tumor viruses.

A single-cell clone of C3Hf mammary tumor cells (clone 14) was developed into a continuous cell line expressing high levels of endogenous mouse mammary tumor virus (MMTV) with less than 0.1% murine leukemia virus expression. Comparison of the C3Hf MMTV protein profile on sodium dodecyl sulfatepolyacrylamide gel electrophoresis with that of C3H MMTV revealed that the protein content of the two viruses was quite similar. However, oligonucleotide fingerprints obtained of MMTV 70S RNA revealed that approximately 20% of the large oligonucleotides examined were unique to each virus. The oligonucleotide fingerprint indicated that although the viruses were similar, they differed in their genetic content. The differences in the two viruses extended to immunological differences in the major envelope glycoprotein, gp52. C3Hf MMTV competed only partially in a homologous radioimmunoassay for gp52 of C3H MMTV, whereas C3H MMTV gave complete competition, indicating that gp52 of C3H MMTV contained type-specific determinants not present on gp52 of C3Hf MMTV. Comparison of C3Hf MMTV with highly oncogenic C3H, GR, and RIII MMTVs in a homologous C3H MMTV gp52 assay gave two patterns of reactivity: complete competition by GR and C3H MMTV and incomplete competition by C3Hf and RIII MMTV. Absorption of anti-C3H MMTV serum by either C3Hf MMTV or RIII MMTV removed all antibodies against both viruses but not against GR and C3H MMTVs. These results indicate that C3H and GR MMTVs are more closely related to each other than to RIII and C3Hf MMTVs.

Animals↗