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At least 1,117 records · Page 62Linked to original sources
PubMed1996

Characterization of anti-mouse IL-12 monoclonal antibodies and measurement of mouse IL-12 by ELISA.

Enzyme-linked immunosorbent assays (ELISAs) capable of quantitatively measuring pg/ml amounts of mouse IL-12 (moIL-12) were developed as an alternative to the current bioassay procedure used for the measurement of moIL-12. A panel of 40 rat anti-moIL-12 monoclonal antibodies were identified and tested for their ability to bind 125I-moIL-12. Two of the MAbs, 2B5 and 9A5, were able to capture 125I-moIL-12 in the presence of unlabelled moIL-12 p35 and moIL-12 p40, suggesting specificity for the moIL-12 p75 heterodimer. Western blot analysis confirmed that MAb 9A5 specifically recognized only moIL-12 p75. Using MAb 9A5, and an additional anti-moIL-12 p40 MAb 5D9, we developed quantitative ELISAs for the specific detection of moIL-12 p75 and p40, respectively. These ELISAs detect moIL-12 with a sensitivity of 40 pg/ml. Whereas the p40 ELISA detected three forms of moIL-12 (p40 monomer, p40 homodimer, and the heterodimer), the p75 ELISA only detected moIL-12 heterodimer. Neither of these assays crossreacted with a panel of additional cytokines. The levels of moIL-12 measured by the p75 ELISA and the bioassay were directly compared and found to correlate well. Therefore, the p75 ELISA represents an alternative to the bioassay for the measurement of moIL-12.

Animals↗
PubMed1987

Studies on radiation-induced chromosome aberrations in mouse spermatocytes. I. Stage specificity and dose-response relationships of chromosome aberrations induced in mouse primary spermatocytes following X-irradiation.

The cytological analysis of chromosome aberrations induced at diplotene, mid-pachytene, zygotene and leptotene stages following X-irradiation was performed at diakinesis-metaphase I in mouse spermatocytes. The dose-response relationships fitted well to linear equations for deletion-type aberrations at each stage, and to linear-quadratic equations for exchange-type aberrations at all stages except for leptotene. The radiosensitivity to chromosome aberration induction tended to increase gradually with progression through synaptic and post-synaptic stages, diplotene being the most sensitive. Chromatid exchanges were hardly observed at leptotene, the aberrations being mainly isochromatid fragments. On the contrary, chromatid exchanges and isochromatid deletions were mainly observed at later stages (zygotene-diplotene). The specificity of chromosome aberration induction in primary spermatocytes might be influenced by chromatin organization and chromosomal configuration peculiar to meiotic cells.

Animals↗
PubMed1991

ENU mutagenesis in the mouse electrophoretic specific-locus test, 1. Dose-response relationship of electrophoretically-detected mutations arising from mouse spermatogonia treated with ethylnitrosourea.

The mouse electrophoretic specific-locus test for induced germ-cell mutations, was used to determine the response of spermatogonial stem cells to a series of doses of the germ cell mutagen N-ethyl-N-nitrosourea (ENU). Male DBA/2J and C57B1/6J mice were treated with doses of 50, 100, 200 or 250 mg/kg ENU and their progeny screened for electrophoretically-detectable mutations at 32 separate loci. As expected, increasing doses of ENU led to increasing mutant frequencies. The differences in mutant frequencies between treated DBA/2J and C57B1/6J males were not statistically significant.

Alleles↗
PubMed1990

Mouse hepatitis virus ORF 2a is expressed in the cytosol of infected mouse fibroblasts.

A 266-bp fragment of cDNA from within gene B, ORF 2a, of MHV-A59 was used to construct a vector encoding a bacterial/viral fusion protein. Antiserum raised against this fusion protein specifically immunoprecipitates a 30K protein from infected 17Cl-1 mouse fibroblasts. The protein is localized primarily in the cytosol and not in the membranes. This is consistent with its predicted sequence and potential role as an RNA binding protein.

Animals↗
PubMed1984

Regulation of stage-specific gene expression during early mouse development: effect of cytochalasin B and aphidicolin on stage-specific protein synthesis in mouse eggs.

Mechanisms regulating stage-specific translation in mouse embryos were studied by inhibitor experiments. When fertilized eggs were continuously treated with cytochalasin B, cleavage was prevented, whereas karyokinesis proceeded, resulting in protein synthesis patterns changing stage-specifically as in control embryos through preimplantation development. When fertilized eggs were continuously exposed to aphidicolin, cleavage and DNA synthesis were inhibited, thus keeping their protein synthesis at the level of fertilized eggs with few new polypeptides appearing after one day. The next day these eggs stopped translation almost completely. Stage-specific translation therefore might be controlled by nuclear replications rather than by cytoplasmic clock.

Animals↗
PubMed1993

Interleukin-6 induction in vitro in mouse brain endothelial cells and astrocytes by exposure to mouse hepatitis virus (MHV-4, JHM).

Interleukin-6 (IL-6) induction, as detected by bioassay and Northern analysis, was examined in vitro in endothelial cells or astrocytes derived from BALB/c (susceptible) or SJL (resistant) mice following exposure to mouse hepatitis virus (MHV-4) or UV inactivated MHV-4 (UV-MHV-4). In BALB/c endothelial cells, up to 16-fold more IL-6 (> 640 U/ml) was induced, compared to SJL cells which showed a minimal response (40 U/ml), relative to basal levels (< 20 U/ml). In contrast, both BALB/c and SJL astrocytes showed a substantial IL-6 response to MHV-4 and UV-MHV-4 exposure, although a strain difference persisted. Despite strain and cell specific differences in released IL-6, equivalent levels of IL-6 mRNA were induced in all cell types following exposure to MHV-4 or UV-MHV-4.

Animals↗
PubMed1993

Abnormal synaptic architecture in the cerebellar cortex of a new dystonic mutant mouse, Wriggle Mouse Sagami.

The 'Wriggle Mouse Sagami (WMS)' is a new neurological mutant with severe dystonic movements of the trunk and extremities whose pathological characters are transmitted by an autosomal recessive gene (wri). Manifestations first appear at 10 days to 2 weeks after birth and progress until 12 weeks of age. In spite of the severe dystonic movements, no marked abnormalities had been found in the cyto- or myeloarchitecture of the central nervous system or that of the peripheral nerves, except for the impaired development of the dendritic trees of the Purkinje cells. In this study we quantitatively demonstrated decreased synaptic connections of parallel fibers on the dendritic spines of the Purkinje cells as early as 2 weeks after birth. On the other hand, synaptic boutons on the dendritic shafts and somata of the Purkinje cells and synaptic bouton-like structures which contained synaptic vesicles but without synaptic membrane specialization, were significantly increased in the molecular layer at 9 weeks of age. Glutamic acid decarboxylase immunohistochemistry suggested that some of these increased synaptic boutons and other bouton-like structures may have originated in GABA interneurons, such as stellate cells, basket cells and Golgi cells, and in the cerebellar nuclei. Because of the severity of the manifestations, it appears that synaptic alteration in interneurons also occurs in the other parts of the CNS.

Animals↗
PubMed1994

Second messenger regulation of mouse gonadotropin-releasing hormone gene expression in immortalized mouse hypothalamic GT1-3 cells.

Using a transgenic mouse derived GnRH expressing neuronal cell line, GT1-3, we studied the effects of activation of cAMP, Ca2+ and protein kinase C pathways by forskolin, ionomycin and the phorbol ester phorbol 12-myristate 13-acetate (PMA), respectively, upon gonadotropin-releasing hormone (GnRH) secretion, cellular peptide content, mRNA and RNA primary transcript levels. Forskolin, ionomycin and phorbol ester all caused an increase in GnRH secretion in GT1-3 cells in a time and dose-dependent manner during a short-term (1 h) static incubation. Prolonged treatment with forskolin (10 microM), ionomycin (1 microM) and PMA (10 nM) for 12 or 24 h resulted in significant decreases in GnRH mRNA levels. Time-course studies showed that the increases in GnRH secretion stimulated by forskolin, ionomycin and PMA were gradually attenuated over time in parallel with the decreases in mRNA expression. In contrast, there were only small and variable changes in the GnRH cellular content. Studies using a GnRH antagonist (100 microM) suggested that the released GnRH has a negative feedback effect on its own secretion. However, co-incubation with the GnRH antagonist did not alter the inhibitory effects on GnRH mRNA levels by the secretagogues. Further studies on the transcriptional effects of forskolin, ionomycin and PMA on GnRH gene expression in GT1-3 cells revealed that all three secretagogues suppressed GnRH RNA primary transcript levels, with forskolin having a slower time course of action. Thus, the inhibition of cytoplasmic GnRH mRNA, and presumably its synthesis, after 12-24 h of secretagogue treatment may be due at least in part to a suppression of GnRH gene transcription.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Presence in mouse Sertoli cell-conditioned medium of a factor that expresses AVP-like inhibition of steroidogenesis by mouse Leydig cells in long-term culture.

The influence of spent medium from immature mouse Sertoli cells (SCM) on testosterone production by purified Leydig cells was investigated and compared to that of AVP, a potent local modulator of Leydig cell steroidogenesis. SCM inhibited in a dose-dependent manner the hCG-stimulated testosterone production, but was ineffective in basal conditions. As is known for AVP, (i) a lag period of 72 h was prerequisite for SCM to inhibit Leydig cell function; (ii) the main effect of SCM was located at a step beyond the receptor-adenylate cyclase system, since the hCG- and 8-bromo-cAMP-stimulated testosterone productions were similarly affected. The possibility that the effect of SCM may be related to AVP-like molecule(s) is also supported by the observations that at maximal concentrations the inhibitory effects of AVP and SCM were not additive and that the inhibition of testosterone production was largely (65%) reversed by the presence of [(beta-mercapto-beta, beta-cyclopentamethylenepropionyl, O-Me-Tyr2,Arg8)-vasopressin], a selective vasopressor antagonist. These data indicate that Sertoli cells produce in vitro potent inhibitory factors of Leydig cell steroidogenesis. They provide additional evidence that one of these bioactive factors has an effect on Leydig cell function similar to that of AVP.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1996

Mouse G2-GPI AChE is processed as a membrane-bound ectoenzyme in transfected mouse sarcoma cells but is not a homophilic adhesion molecule.

Acetylcholinesterase (AChE) is mainly involved in synaptic transmission by hydrolyzing acetylcholine in the synaptic cleft. It has been suggested that it could also be involved in other functions such as cell-cell adhesion. In this study, we have expressed mouse G2-GPI AChE at the membrane surface of S180 cells. We obtained a transfected cell line which permanently expresses high levels of AChE at the cell surface. However, transfected cells behave as single cells in culture. We performed cell aggregation and adhesion tests and found no significant aggregation or adhesion, which suggests that AChE is not a homophilic adhesion molecule.

Acetylcholinesterase↗
PubMed1996

Complement gene expression in mouse microglia and astrocytes in culture: comparisons with mouse peritoneal macrophages.

We investigated the mRNA expression of the various complement components in cultured mouse microglia and astrocytes by the reverse transcription and polymerase chain reaction. C1q, C2, C3, and C4 mRNAs were detected in microglial cultures. C3 and C4 mRNAs were found in astrocyte cultures. Microglia showed enhanced expression of C2, C3, and C4 mRNAs when they were treated with lipopolysaccharide. Much higher expression of C1q, C2, C3, and C4 mRNAs was detected in microglia after stimulation with interferon-gamma. Our data suggest that microglia and astrocytes may produce some of the complement components also in vivo, which can be facilitated in certain infectious and inflammatory diseases in the central nervous system.

Animals↗
PubMed1994

Antinociception following implantation of mouse B16 melanoma cells in mouse and rat spinal cord.

B16 F1C29 melanoma cells, which are thought to contain and release catecholamines, were implanted in mouse and rat spinal subarachnoid space. B16 F1C29 cell implants augmented the antinociceptive effect of morphine in tail-flick test, and this interaction was blocked by either the alpha 2-adrenergic antagonist idazoxan or the opioid antagonist naloxone. B16 F1C29 cell implants also augmented the antinociceptive effect of the catecholamine re-uptake blocker desipramine. Substance P-induced biting and scratching behaviors were inhibited in mice receiving B16 F1C29 cell implants, and this effect of B16 F1C29 cell implants was blocked by the alpha 2-adrenergic antagonist idazoxan. Mice receiving B16 F1C29 cell implants showed tolerance to intrathecal administration of the alpha 2-adrenergic agonist UK 14304. These results suggest that B16 cell implant-induced antinociception was mediated by catecholamines secreted from the cell implants and acting at spinal alpha 2-adrenergic receptors. Spinal implantation of catecholamine-releasing cells may provide an alternative approach for the therapy of chronic intractable pain and a useful model to study alpha 2-adrenergic receptor tolerance.

Adrenergic alpha-Agonists↗
PubMed1996

Similarities in the age-related hippocampal deposition of periodic acid-schiff-positive granules in the senescence-accelerated mouse P8 and C57BL/6 mouse strains.

With advancing age clusters of abnormal granules positive for periodic acid-Schiff appear in the hippocampus of C57BL/6 (B6) mice and the senescence-accelerated mouse (SAM) P8. The granules can also be visualized with a polyclonal antibody to a 110,000 mol. wt laminin-binding protein and stain specifically with a monoclonal antibody to heparan sulfate proteoglycan. The present study used light and electron-microscopic analysis to compare the staining and morphological properties of these granules in SAM P8 hippocampus with those in B6 hippocampus at different ages. The results of the light-microscopic analysis revealed that granules in SAM P8 and B6 had similar morphology, staining characteristics and distribution patterns, and appeared to have a close association with astrocytic process. The onset of granules in SAM P8 mice (at two to three months of age) was earlier than that observed in B6 mice (at four to six months of age), but the maximum incidence was similar in both strains. Electron-microscopic analysis revealed that the granules in SAM P8 and B6 mice also had a very similar ultrastructure. Granules in both strains were surrounded by a discontinuous membrane and contained mostly crystalline-like, degenerated material. The successive ultrastructural changes from the exterior to interior of the granules suggest that the degenerative process was initiated outside the granules and that degenerative structures migrate inward. Astrocytes and heparan sulfate proteoglycan are closely associated with beta-amyloid deposits in Alzheimer's disease. The presence of astrocyte-associated heparan sulfate proteoglycan-positive material in aged SAM P8 and B6 mice might model age-related alterations in glia function possibly involved in human cerebral amyloidogenesis.

Aging↗
PubMed1988

herpes simplex virus infection accelerates the age-related reactivity of mouse trigeminal ganglia neurons with anti-mouse IgG antibody in immunostaining.

The detection of viral proteins is a major goal of research on herpes simplex virus type 1 (HSV-1) latency. We used immunostaining to detect viral proteins in neuronal cells of trigeminal ganglia of Balb/c mice after corneal inoculation with HSV-1 virus. Viral proteins were detected in the neurons during the acute stage of infection, i.e. within one week after inoculation. However, the detection of viral antigens at the latent stage of HSV-1 infection has proven difficult. We have detected age-dependent non-specific reactivity with anti-mouse IgG antibody in the neurons of 10-week-old or older uninfected mice. This reactivity is accelerated in HSV-1 infected mice, being seen at 6 weeks of age (2 weeks post infection). The accelerated reaction and impact of this effect is discussed in relation to detection of viral proteins during latency.

Aging↗
PubMed1991

The human homolog of the mouse brown gene maps to the short arm of chromosome 9 and extends the known region of homology with mouse chromosome 4.

The mouse brown locus encodes a tyrosinase-related protein, TRP-1. The human homolog of TRP-1 was recently cloned from a melanoma cDNA library and sequenced. We have made oligonucleotide primers corresponding to the human TRP1 3' untranslated region and used them to map the human TRP1 gene by species-specific PCR in human/rodent somatic cell hybrids. By this means, the human TRP1 gene has been mapped to the short arm of chromosome 9.

Animals↗
PubMed1993

The mouse Dlx-2 (Tes-1) gene is expressed in spatially restricted domains of the forebrain, face and limbs in midgestation mouse embryos.

The pattern of RNA expression of the murine Dlx-2 (Tes-1) homeobox gene is described in embryos ranging in age from E8.5 through E11.5. Dlx-2 is a vertebrate homologue of the Drosophila Distal-less (Dll) gene. Dll expression in the Drosophila embryo is principally limited to the primordia of the brain, head and limbs. Dlx-2 is also expressed principally in the primordia of the forebrain, head and limbs. Within these regions it is expressed in spatially restricted domains. These include two discontinuous regions of the forebrain (basal telencephalon and ventral diencephalon), the branchial arches, facial ectoderm, cranial ganglia and limb ectoderm. Several mouse and human disorders have phenotypes which potentially are the result of mutations in the Dlx genes.

Animals↗
PubMed1989

Changes of prostacyclin and thromboxane synthesis in the course of mouse liver perfusion. Stimulated thromboxane A2 synthesis of freshly prepared isolated mouse hepatocytes.

The formation of prostacyclin and thromboxane A2 (measured as 6-keto PGF1 alpha and TXB2 by radioimmunoassay) was investigated during a 30 min perfusion of mouse liver in a recirculation system. After cannulation of the portal vein an immediate increase of de novo synthesis and secretion of PGI2 occurred followed by a sharp decrease. Increased PGI2 synthesis was also followed by a continuous increase of TXA2 synthesis and secretion reaching a maximum at the end of the 30 min perfusion. Elevated TXA2 synthesis was also shown in freshly isolated hepatocytes investigated in the course of a 20 min incubation period immediately after the perfusion. However, the elevated TXA2 formation was not observed when it was measured after a 120 min preincubation of the cells. Both PGI2 and TXA2 production could be provoked to a similar extent by the addition of arachidonate and A 23187 immediately after the perfusion or after a 120 min preincubation.

6-Ketoprostaglandin F1 alpha↗
PubMed2005

Cloning and characterization of mouse disabled 2 interacting protein 2, a mouse orthologue of human NOSTRIN.

The mouse disabled 2 interacting protein 2 (mDaIP2) had been obtained through yeast two hybrid system. It consists of 506 amino acids and its calculated molecular weight is 57.7 kDa. The protein contains N-terminal FCH domain and C-terminal SH3 domain. The SH3 domain interacts with the proline rich domain of mDab2 which had been identified to possess a transcriptional activation function. In RA-treated F9 teratocarcinoma cell, the mDaIP2 and mDab2 genes were differentially expressed in a RA-responsive manner and both were detected to localize in cytoplasm and nucleus. Homology search of all NCBI sequences indicated that the amino acid sequence of mDaIP2 shares 82% identity with human NOSTRIN which controls activity, trafficking, and targeting of nitric oxide synthase (eNos). The eNos was not detected in RA-treated F9 cell. These results suggest that mDaIP2 somehow functions in a different fashion from NOSTRIN in F9 cell differentiation and that its function may be concerted with that of mDab2.

Adaptor Proteins, Signal Transducing↗