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At least 865 records · Page 48Linked to original sources
PubMed2005

Inhibition of prion propagation in scrapie-infected mouse neuroblastoma cell lines using mouse monoclonal antibodies against prion protein.

We screened six mouse monoclonal antibodies (mAbs) against prion protein (PrP), which were previously established in our laboratory, for inhibitory activity against PrP(Sc)-accumulation in scrapie-infected cell lines and identified two mAbs, 3S9 and 2H9, as possessing this inhibitory activity. mAb 3S9 recognized an epitope including 154th tyrosine in the helix 1 region of PrP, while mAb 2H9 recognized a discontinuous region that included helix 1. In three scrapie-infected cell lines infected with different mouse-adapted scrapie strains, mAb 3S9 strongly inhibited accumulation of PrP(Sc), while mAb 2H9 moderately inhibited accumulation of PrP(Sc), indicating that inhibition of prion propagation by mAbs may be dependent on PrP(Sc) characteristics. Furthermore, mAb 3S9 completely excluded PrP(Sc) from these cell lines. These results suggest that mAbs 3S9 and 2H9 might be useful for clarifying the mechanisms of prion propagation and prevention by PrP-specific antibodies, and for tracing the conversion of PrP(C) to other PrP(Sc) isoforms.

Amino Acid Sequence↗
PubMed2005

The mouse immune response to human fibrinogen reveals an autoimmune component against mouse fibrinogen.

The present experiments were carried out to analyze whether immunization of mice with human fibrinogen would induce autoimmunity like other heterologous proteins such as collagen type II, thyroglobulin or myelin basic protein. Our results demonstrate that human fibrinogen induces very strong immune responses in all mouse strains analyzed. Autoimmune responses with short-term memory to mouse fibrinogen are induced in genetically susceptible mice. These autoimmune Th2-type responses induce splenomegaly, enhanced coagulation times, and production of rheumatoid factors. The short-lived autoimmune memory was not regulated by either suppressor T cells or exhaustion of immune cells; rather this potentially dangerous autoimmune response was regulated by unknown, antigen-specific feedback mechanisms (they do not influence immune responses to proteins like HSA and OA in the same mice). Such feedback mechanisms were not found in the immune responses to other heterologous proteins inducing significant cross-reactive autoimmunity such as collagen type II, thyroglobulin, or myelin basic protein.

Animals↗
PubMed2006

Rapid and simultaneous determination of capecitabine and its metabolites in mouse plasma, mouse serum, and in rabbit bile by high-performance liquid chromatography.

A rapid high-performance liquid chromatography method has been developed for simultaneous determination of capecitabine and its metabolites: 5'-deoxy-5-fluorocytidine (5'-DFCR), 5'-deoxy-5-fluorouridine (5'-DFUR) and 5-fluorouracil (5-FU). 5'-DFCR was synthesized by hydrolyzing capecitabine using commercially available carboxyl esterase (CES) and characterized by NMR, mass spectrometry and elemental analysis. Base-line separations between capecitabine, 5'-DFCR, 5'-DFUR and 5-FU were found with symmetrical peak shapes on a Discovery RP-amide C16 column using 10 mM ammonium acetate at pH 4.0 and methanol as the mobile phase. The retention times of capecitabine, 5'-DFCR, 5'-DFUR and 5-FU were 8.9, 5.0, 5.3 and 3.0 min, respectively. Linear calibration curves were obtained for each compound across a range from 1 to 500 microg ml(-1). The intra- and inter-day relative standard deviations (%RSD) were <5%. A single-step protein precipitation method was employed for separation of the analytes from bio-matrices. Greater than 85% recoveries were obtained for capecitabine, 5'-DFCR, 5'-DFUR and 5-FU from bio-fluids including mouse plasma, mouse serum and rabbit bile.

Animals↗
PubMed2006

A novel acoustic evaluation system of scratching in mouse dermatitis: rapid and specific detection of invisibly rapid scratch in an atopic dermatitis model mouse.

Scratching is an essential and a skin specific behavior induced by itching, which is a common symptom of atopic dermatitis (AD) and other types of dermatitis. Itching sensation and scratching are closely associated and thus scratching times are currently used for evaluating itching in animal models. However, objective measuring systems of scratching to assess the grade of dermatitis and the effectiveness of anti-pruritic drugs in animal dermatitis models are lacking. To investigate a quantitative evaluation system for itching, we have developed a novel acoustic scratching counting system and compared its accuracy with time-consuming slow-motion video recording system. We have also objectively evaluated the efficacy of an antihistamine using this novel system. Scratching behavior of an AD model mouse (K14 driven IL-18 transgenic mouse) was recorded visually and acoustically. Specific scratching sound produced by mice was recorded and counted using a software we have developed, and the results obtained using our acoustic system were not statistically different from data obtained using slow motion video system. Surprisingly, mice scratched more than 10 times/second, which was invisibly rapid motion and revealed inaccuracy of conventional hand counting system. Results were identical to that of measured by 10 times time costing slow-motion video analysis. The antihistamine is clearly effective for suppression of scratching as demonstrated using this objective and accurate method. This novel motion analysis system will open a window for physiological and pathological analysis for animal models and development of anti-pruritic drugs.

Animals↗
PubMed2005

Orthovanadate increased the frequency of aneuploid mouse sperm without micronucleus induction in mouse bone marrow erythrocytes at the same dose level.

The objective of the current study was to investigate the ability of orthovanadate to induce aneuploidy in mouse sperm and micronuclei in mouse bone marrow cells at the same dose levels. The BrdU-incorporation assay was performed to test if the chemical treatment altered the duration of the meiotic divisions. It was found that orthovanadate (25mg/kg bw) treatment did not cause meiotic delay. To determine the frequencies of hyperhaploid and diploid sperm, male mice were treated by intraperitoneal (i.p.) injection with 5, 15 or 25mg/kg bw orthovanadate and sperm were sampled from the Caudae epididymes 22 days later. Fluorescence in situ hybridization (FISH) was performed with DNA-probes for chromosomes 8, X or Y. Significant increases in the frequencies of total hyperhaploid sperm (p<0.01) were found with 15 and 25mg/kg bw orthovanadate, indicating induced non-disjunction during male meiosis. The dose-response was described best by a linear equation. Orthovanadate did not significantly increase the frequencies of diploid sperm at any of the three doses tested, indicating that no complete meiotic arrest occurred. Orthovanadate was investigated also by the micronucleus test at i.p. doses of 1, 5, 15 or 25mg/kg bw, followed by bone marrow sampling 24h after treatment. None of the orthovanadate doses caused a significant increase in the rates of micronuclei (MN). Since the results show that orthovanadate induced non-disjunction during male meiosis without an accompanying induction of MN in bone marrow erythrocytes under the present experimental conditions and doses, it is concluded that male germ cells (meiosis) are more sensitive to the aneugenic effects of orthovanadate than somatic cells (mitosis). However, induction of micronuclei was reported in the literature with orthovanadate, vanadylsulfate and ammonium metavanadate, which contradicts the notion that vanadium compounds might be unique germ cell aneugens.

Aneugens↗
PubMed2006

Spastin in the human and mouse central nervous system with special reference to its expression in the hippocampus of mouse pilocarpine model of status epilepticus and temporal lobe epilepsy.

In the present in situ hybridization and immunocytochemical studies in the mouse central nervous system (CNS), a strong expression of spastin mRNA and protein was found in Purkinje cells and dentate nucleus in the cerebellum, in hippocampal principal cells and hilar neurons, in amygdala, substantia nigra, striatum, in the motor nuclei of the cranial nerves and in different layers of the cerebral cortex except piriform and entorhinal cortices where only neurons in layer II were strongly stained. Spastin protein and mRNA were weakly expressed in most of the thalamic nuclei. In selected human brain regions such as the cerebral cortex, cerebellum, hippocampus, amygdala, substania nigra and striatum, similar results were obtained. Electron microscopy showed spastin immunopositive staining in the cytoplasma, dendrites, axon terminals and nucleus. In the mouse pilocarpine model of status epilepticus and subsequent temporal lobe epilepsy, spastin expression disappeared in hilar neurons as early as at 2h during pilocarpine induced status epilepticus, and never recovered. At 7 days and 2 months after pilocarpine induced status epilepticus, spastin expression was down-regulated in granule cells in the dentate gyrus, but induced expression was found in reactive astrocytes. The demonstration of widespread distribution of spastin in functionally different brain regions in the present study may provide neuroanatomical basis to explain why different neurological, psychological disorders and cognitive impairment occur in patients with spastin mutation. Down-regulation or loss of spastin expression in hilar neurons may be related to their degeneration and may therefore initiate epileptogenetic events, leading to temporal lobe epilepsy.

Adenosine Triphosphatases↗
PubMedDate not supplied

Teratoma formation and hepatocyte differentiation in mouse liver transplanted with mouse embryonic stem cell-derived embryoid bodies.

We previously reported that mouse embryonic stem (ES) cells are capable of differentiating into hepatocytes in cultured embryoid bodies (EBs) and that hepatocytes generate in the recipient liver injected with cultured day-9 EB cells via spleen without the formation of a teratoma. Because ES cells frequently form teratomas in recipient mice, we investigated incidence of teratoma formation when day-9 EBs derived from ES cells were transplanted directly into the subcapsule of mouse liver. In contrast to injection of day-9 EB cells through the portal vein via the spleen, direct subcapsular injection of cultured day-9 EB cells into liver, and even of cultured day-15 EBs, resulted in an high incidence of teratoma in the liver. In teratomas of livers injected directly with day-15 EBs, hepatocytes were detected singly and in clusters. These results imply that undifferentiated cells capable of developing into teratomas exist in cultured EBs, and even in cultured day-15 EBs containing differentiated hepatocytes.

Animals↗
PubMed2005

Mouse cDNA microarray analysis uncovers Slug targets in mouse embryonic fibroblasts.

There is a need to reveal mechanisms that account for maintenance of the mesenchymal phenotype in normal development and cancer. Slug (approved gene symbol Snai2), a member of the Snail gene family of zinc-finger transcription factors, is believed to function in the maintenance of the nonepithelial phenotype. This study identified candidate Slug target genes linked to Slug gene suppression in primary mouse embryonic fibroblasts. Expression analyses were performed with a mouse cDNA microarray (Mousechip-CNIO) containing 15,000 clones. A total of 15 novel Slug target species were validated by real-time PCR or Western analyses. These included self-renewal genes (Bmi1, Nanog, Gfi1), epithelial-mesenchymal genes (Tcfe2a, Ctnb1, Sin3a, Hdac1, Hdac2, Muc1, Cldn11), survival genes (Bcl2, Bbc3), and cell cycle/damage genes (Cdkn1a, Rbl1, Mdm2). Expression patterns were studied in wild-type MEFs and Slug-deficient MEFs. Slug-complementation studies recovered aberrant gene expression in cells lacking Slug, indicating that these genes were regulated directly by Slug. These results highlight their potential roles in mediating Slug function in mesenchymal cells and may help to identify novel therapeutic biomarkers in cancers linked to Slug.

Animals↗
PubMed2001

Mitochondrial alterations caused by defective peroxisomal biogenesis in a mouse model for Zellweger syndrome (PEX5 knockout mouse).

Zellweger syndrome (cerebro-hepato-renal syndrome) is the most severe form of the peroxisomal biogenesis disorders leading to early death of the affected children. To study the pathogenetic mechanisms causing organ dysfunctions in Zellweger syndrome, we have recently developed a knockout-mouse model by disrupting the PEX5 gene, encoding the targeting receptor for most peroxisomal matrix proteins (M Baes, P Gressens, E Baumgart, P Carmeliet, M Casteels, M Fransen, P Evrard, D Fahimi, PE Declercq, D Collen, PP van Veldhoven, GP Mannaerts: A mouse model for Zellweger syndrome. Nat Genet 1997, 17:49-57). In this study, we present evidence that the absence of functional peroxisomes, causing a general defect in peroxisomal metabolism, leads to proliferation of pleomorphic mitochondria with severe alterations of the mitochondrial ultrastructure, changes in the expression and activities of mitochondrial respiratory chain complexes, and an increase in the heterogeneity of the mitochondrial compartment in various organs and specific cell types (eg, liver, proximal tubules of the kidney, adrenal cortex, heart, skeletal and smooth muscle cells, neutrophils). The changes of mitochondrial respiratory chain enzymes are accompanied by a marked increase of mitochondrial manganese-superoxide dismutase, as revealed by in situ hybridization and immunocytochemistry, suggesting increased production of reactive oxygen species in altered mitochondria. This increased oxidative stress induced probably by defective peroxisomal antioxidant mechanisms combined with accumulation of lipid intermediates of peroxisomal beta-oxidation system could contribute significantly to the pathogenesis of multiple organ dysfunctions in Zellweger syndrome.

Adenosine Triphosphate↗
PubMed2002

Generation of neutralizing mouse anti-mouse IL-18 antibodies for inhibition of inflammatory responses in vivo.

The proinflammatory cytokine IL-18 mediates IFN-gamma production as well as the induction of Th1 polarized immune responses in synergy with IL-12. In this study, we describe the production of isogeneic monoclonal antibodies (Mabs) directed against murine IL-18 (mIL-18). Immunization of IL-18-deficient mice with recombinant mIL-18 in the presence of CpG-oligodeoxynucleotides (CpG-ODN) and alum as adjuvant resulted in high anti-IL-18 serum titers. We could identify two Mabs, SK721-2 and SK113AE-4, which were able to bind to IL-18 and neutralize its IFN-gamma inducing effect in vitro with an IC(50) of 40-100 ng/ml. In vivo, LPS-induced IFN-gamma production was reduced by 60-85% following a single administration of Mabs SK113AE-4 or SK721-2. Since IL-18 is likely to be involved in the pathogenesis of inflammatory diseases such as rheumatoid arthritis or Crohn's disease, neutralizing mouse anti-mouse IL-18 Mabs have the potential to become valuable tools for the therapeutic exploration of long-term IL-18 blockade in vivo.

Adjuvants, Immunologic↗
PubMed1990

In vitro and in vivo anti-tumor activity of recombinant mouse tumor necrosis factor (TNF) in a mouse bladder tumor (MBT-2).

Tumor necrosis factor (TNF) has confirmed anti-tumor activity. When used in combination with interferon gamma (IFNG) or chemotherapeutic drugs targeted at DNA topoisomerase II, synergistic cytotoxicity has been observed. Investigations of the anti-tumor activity of recombinant mouse TNF in a mouse bladder tumor model (MBT-2) were performed. The cytotoxicity of TNF and low dose actinomycin-D (AMD) against MBT-2 in vitro was examined alone and following preincubation with IFNG. The activity of TNF/AMD in vivo utilizing an intravesical implantation mode (MBT-2) was also evaluated. TNF alone had no cytotoxic effect in vitro. TNF/AMD was cytotoxic for MBT-2 growth in vitro. Maximum cytotoxicity (86%) occurred at one microgram./ml. TNF/one microgram./ml. AMD with 50% cytotoxicity at .64 micrograms./ml. TNF/one/microgram./ml. AMD. A two hour preincubation with IFNG markedly increased the cytotoxicity of TNF/AMD whereas longer incubations did not enhance cytotoxic activity. TNF alone and in combination with AMD did not significantly reduce the percentage of intravesical tumor outgrowth in vivo compared to controls. This study demonstrated that TNF/AMD exhibits cytotoxicity for MBT-2 cells in vitro but is ineffective in reducing implantation of intravesical tumors in vivo. The in vitro data suggest brief exposure of MBT-2 cells to IFNG augments the subsequent anti-tumor activity of TNF/AMD.

Administration, Intravesical↗
PubMed1998

Comparison between in vivo mutagenicity and carcinogenicity in multiple organs by benzo[a]pyrene in the lacZ transgenic mouse (Muta Mouse).

To evaluate whether the in vivo mutagenicity test system using the lacZ transgenic mice (Muta Mouse) may be applied to carcinogenesis studies, both the in vivo mutagenicity and carcinogenicity of benzo[a]pyrene (BP) was tested in mice under the same administration conditions. The eleven organs of the mice on the 14th day after the final oral administration of BP at a dose of 125 mg kg(-1) day(-1) or corn oil for 5 consecutive days were tested for in vivo mutation by the positive-selection method. The data show that the colon had the highest lacZ mutant frequency (37-fold increase over the spontaneous frequency), followed by the ileum > forestomach > bone marrow, spleen > glandular stomach > liver, lung > kidney and heart. No significant mutations were found in the brain. These results may suggest that, in general, the organs with rapidly proliferative tissues have a marked increase in vivo mutant frequencies under the conditions of this experimental design. The forestomach and lymphatic organs including the spleen (malignant lymphoma) were the main target organs for BP carcinogenesis by 5 daily oral doses of 75 and 125 mg kg(-1) day(-1). These results suggest that the mutation results from the transgenic assay with BP reflect the carcinogenicity of BP in the mouse. They also indicate, however, that the magnitude of the in vivo lacZ mutant frequencies induced by BP in different organs did not fully correlate with the target organs for carcinogenicity.

Animals↗
PubMed1999

Multiple organ mutation in the lacZ transgenic mouse (Muta mouse) 6 months after oral treatment (5 days) with benzo[a]pyrene.

We have recently demonstrated that not all organs with high rates of mutation in the lacZ transgene develop tumors using the Muta Mouse. To better understand the role of in vivo mutation in carcinogenesis, we examined the mutant frequencies (MF) of the lacZ transgene in tumor-bearing and non tumor-bearing organs. MF, recovered after 2 weeks (the data taken from our previous study) and after 26 weeks following oral doses of 125 mg kg-1 day-1 benzo[a]pyrene (BP) for five days were compared. The organs examined included the target organs (forestomach, spleen, and lung) and non-target organs (colon, glandular stomach, and liver) for BP carcinogenesis. The data indicated that lacZ MF were markedly increased over spontaneous frequencies in the organs examined and that the organ which showed the highest MF was the colon, followed by the forestomach>spleen>glandular stomach, liver, and lung in that order. These findings indicate that the MF of the lacZ transgene in each organ, even 26 weeks after the start of the treatment does not fully correlate with the known target organs of BP. Furthermore, the lacZ MF in a non-papilloma region of a forestomach with a papilloma was equivalent to the two highest MF observed in the healthy colon (non-target organ) of mice at 26 weeks. These observations also indicate that the generation of tumors requires the induction of mutations as well as other factor(s) specific to the target organs. These results clearly suggest that highly mutated organs do not always progress to tumors in the transgenic mouse.

Administration, Oral↗
PubMed1992

Behaviour of mouse macrophage cell line and mouse fibroblast on copolymers containing cellulose triacetate.

Copolymers containing cellulose triacetate were prepared under various conditions. A bacteriological plastic dish was coated with the copolymer (HCTA-MDI copolymer) composed of hydrolysed cellulose triacetate (HCTA) and diphenylmethane diisocyanate (MDI). The deacetylated copolymer (DA-copolymer) was prepared by the deacetylation of HCTA-MDI copolymer. The behaviour of animal cells such as a mouse macrophage cell line (A640-BB-2 cells) and a mouse fibroblast (3T6 cells) on prepared dishes was investigated morphologically. A640-BB-2 cells showed good adhesion and smooth spreading, and 3T6 cells also showed good adhesion and sufficient cell growth on the dish coated with HCTA-MDI copolymer. These results suggest that these copolymers are useful for biomedical materials.

Animals↗
PubMed1996

Mutagenicity to the mouse bone marrow by the mouse germ cell mutagen N-propyl-N-nitrosourea.

N-Propyl-N-nitrosourea (PNU) is shown to be active in male mouse bone marrow micronucleus assays when dosed at either 100 or 200 mg/kg in saline. Activity was observed following either intraperitoneal (i.p.) injection or oral gavage. This observation is consistent with the demonstration by Murota and Shibuya of the specific-locus mutagenicity caused by PNU in male mouse spermatogonia when dosed at 200 mg/kg by i.p. injection. These data strengthen further the observation that rodent germ cell mutagens are also mutagenic to rodent somatic cells.

Animals↗
PubMed2003

Cloning of mouse Ca2+/calmodulin-dependent protein kinase kinase beta (CaMKKbeta) and characterization of CaMKKbeta and CaMKKalpha distribution in the adult mouse brain.

The Ca(2+)/calmodulin-dependent protein kinase kinases alpha and beta (CaMKKs alpha and beta) are novel members of the CaM kinase family. The CaMKKbeta was cloned from mouse brain. The deduced amino acid sequence shared 96.43% homology with the rat CaMKKbeta. Both the alpha and beta isoforms were widely distributed throughout the adult mouse brain. Additionally, all peripheral tissues examined displayed CaMKK alpha and beta expression.

Animals↗
PubMed1984

Induction of natural killer cells and interferon during mouse hepatitis virus infection of resistant and susceptible inbred mouse strains.

Following infection by mouse hepatitis virus (JHM strain), an induction of natural killer (NK) cell activity was observed in C3H mice, which are considered to be sensitive to JHM virus infection. In contrast, mice of the resistant SJL strain did not show any increase of NK cell activity after JHM virus infection. However, infection of both SJL and C3H mice with mouse hepatitis virus type 3 (MHV3) resulted in an increase of NK level, comparable to that observed with the JHM virus infection in the C3H strain. No significant differences were observed in the NK cell activity of the peritoneal exudate or spleen cells of infected mice. Low levels of interferon were detected in serum or peritoneal exudate of C3H mice infected with JHM virus 18 or 24 hours before, but no detectable early interferon production was found. Also no interferon could be detected in the resistant SJL mice. After JHM virus infection, the number of peritoneal exudate cells (PEC) was increased significantly in C3H mice but not in SJL mice. Macrophages obtained from the C3H mice supported virus replication, whereas SJL macrophages did not. Our data suggest that NK cells do not play a role in the resistance of SJL mice against JHM virus infection but may participate in the defence mechanisms against this virus in C3H mice.

Animals↗
PubMed1987

Differential expression of the HLA-B7 and the HLA-A2 gene in transfected mouse L(tk-) cells after stimulation by mouse interferon.

Mouse L(tk-) cells were transfected with recombinant genomic clones encoding the human major histocompatibility antigens HLA-A2 or HLA-B7. The exposure of 15 different transfected cell clones to mouse interferon resulted in an up to 2.9-fold enhancement of the HLA-A2 antigen at the cell surface but in an up to 5.5-fold enhancement of the HLA-B7 antigen as shown by quantitative radioimmunoassay with monoclonal antibodies directed against different HLA epitopes. Using the HLA-Bw6 specific monoclonal antibody 2BC4, an even higher increase of the HLA-B7 antigen (up to 12-fold) could be observed. This higher inducibility of an HLA-B versus HLA-A locus gene may reflect distinct regulatory mechanism controlling the expression of HLA class I subregion antigens.

Animals↗