References of "Rentier, Bernard"
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See detailExperimental models to study measles virus persistence in the nervous system
Rammohan, K. W.; Dubois-Dalcq, M.; Rentier, Bernard ULg et al

in Progress in Neuropathology (1983), 5

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See detailFibronectin promotes rat Schwann cell growth and motility
Baron-Van Evercooren, Anne; Kleinman, Hinda K.; Seppa, H. E. et al

in Journal of Cell Biology (1982), 93(1), 211-216

Techniques are now available for culturing well characterized and purified Schwann cells. Therefore, we investigated the role of fibronectin in the adhesion, growth, and migration of cultured rat Schwann ... [more ▼]

Techniques are now available for culturing well characterized and purified Schwann cells. Therefore, we investigated the role of fibronectin in the adhesion, growth, and migration of cultured rat Schwann cells. Double-immunolabeling shows that, in primary cultures of rat sciatic nerve, Schwann cells (90%) rarely express fibronectin, whereas fibroblasts (10%) exhibit a granular cytoplasmic and fibrillar surface-associated fibronectin. Secondary cultures of purified Schwann cells do not express fibronectin. Exogenous fibronectin has a small effect on promoting the adhesion of Schwann cells to the substrate and does not significantly affect cell morphology, but it produced a surface fibrillar network on fibronectin on the secondary Schwann cells. Tritiated thymidine autoradiography revealed that addition of fibronectin to the medium, even at low concentrations, markedly stimulates Schwann cell proliferation, in both primary and secondary cultures. In addition, when cell migration was measured in a Boyden chamber assay, fibronectin was found to moderately, but clearly, stimulate directed migration or chemotaxis. [less ▲]

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See detailAcute and persistent viral infections of differentiated nerve cells
Dubois-Dalcq, Monique; Rentier, Bernard ULg; Hooghe-Peters, Elisabeth L. et al

in Reviews of Infectious Diseases (1982), 4(5), 999-1014

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See detailSchwann cells in vitro
Rentier, Bernard ULg

in Archives de Biologie (1982), 93

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See detailEtude de l'infection rougeoleuse in vitro et de sa persistance dans les cellules nerveuses en culture
Rentier, Bernard ULg

Thèse d’agrégation de l’enseignement supérieur (1982)

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See detailChronic measles virus infection of mouse nerve cells in vitro
Rentier, Bernard ULg; Claysmith, A. P.; Dubois-Dalcq, Monique et al

in Bishop, David H. L.; Compans, Richard W. (Eds.) The replication of negative strand viruses : proceedings of the 4th International Symposium on Negative Strand Viruses held October 26-November 1, 1980 at Frenchman’s Reef, Saint Thomas, U.S. Virgin Islands (1981)

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See detailEtude de l'infection rougeoleuse in vitro et de sa persistance dans les cellules nerveuses en culture
Rentier, Bernard ULg

in Bulletin de l'Institut Pasteur (1981), 79(2), 107-170

Measles virus can infect neurons in culture. In mouse fetal neurons, infection is spontaneously persistent. Reactivation occurs very rarely. In human fetal neurons, infection is persistent if cells are ... [more ▼]

Measles virus can infect neurons in culture. In mouse fetal neurons, infection is spontaneously persistent. Reactivation occurs very rarely. In human fetal neurons, infection is persistent if cells are cultured in human serum. However, if serum-free medium is used, infection becomes lytic and productive.Latency in mouse neurons is apparently due to the species barrier while latency in human neurons is induced by anti-measles virus antibodies contained in the serum. This might explain the difference between measles encephalitis and subacute sclerosing panencepalitis (SSPE), with presence of anti-measles antibody in the brain in the latter and not in the former. [less ▲]

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See detailStructure and behavior of rat primary and secondary Schwann cells in vitro
Dubois-Dalcq, Monique; Rentier, Bernard ULg; Baron-Vanevercooren, Anne et al

in Experimental Cell Research (1981), 131(2), 283-297

The structure and motility of isolated rat primary (I) Schwann cells (SC) have been compared to that of subcultured (II) SC during and after mitotic stimulation. I SC contain myelin components which ... [more ▼]

The structure and motility of isolated rat primary (I) Schwann cells (SC) have been compared to that of subcultured (II) SC during and after mitotic stimulation. I SC contain myelin components which persist for 2 weeks in serum-free medium while they rapidly disappear in medium containing serum and high glucose concentration. These components were never detected in II SC. Both I SC and II SC after their mitotic phase are spindle-shaped, contain many intermediate and actin filaments, have no basement membrane but show intense migratory and undulatory activities. Rare fibroblasts in I cultures are recognized by their extremely variable shape, the presence of Thy 1.1 antigen in their membrane and their intense edge ruffling alternating with abrupt translocation. In contrast, I SC movements consist of intracellular translocation of nuclei along SC processes, which retract and extend constantly, and in slow rhythmic undulation episodes (2.3 ± 0.2/min) alternating with migration at 135 ± 50 μ/h. The total number of these episodes per day in serum-free medium is rigorously identical for different cells (166.3 ± 0.2) and this uniformity of frequency suggests a genotypic basis. Cycles, consisting of an undulation episode followed by a resting interval, have mean durations of 8.6 ± 4.1 min and a sharp peak of occurrence at 6 min, with exponential distribution of the longer periods. Motility of II SC is considerably inhibited during mitotic stimulation by cholera toxin and a pituitary extract while SC phenotype has changed to a flat multipolar cell with prominent Golgi and ribosomes. Migration is reduced to 24 ± 2 μ/h and only 2% of the SC show pulsations of the same periodicity as the I SC undulations. A dramatic increase in pulsation frequency occurs 6–12 h after removal of mitogenic factors when 80% of II SC start pulsating twice as fast for 2–3 days. When mitoses cease, SC quickly recover their SC phenotype with rhythmic undulations while migration speed increased to 92 ± 20 μ/h. Thus, in spite of dramatic modification of shape, structure and behavior during mitotic stimulation, SC subsequently recover their unique motility pattern which might be essential for their myelinating function [less ▲]

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See detailPreservation of pulsory and migratory activities of rat Schwann cells before and after mitotic stimulation
Rentier, Bernard ULg; Dubois-Dalq, Monique; Baron-Van Evercooren, A.

in Abstracts - Society for Neuroscience (1980)

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See detailSelective and persistent measles virus infection of mouse neurons in vitro
Rentier, Bernard ULg; Claysmith, A. P.; Dubois-Dalcq, Monique et al

in Journal of Neuropathology and Experimental Neurology (1980), 39(3), 185-185

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See detailScanning and transmission electron microscopy study of antibody-dependent lymphocyte-mediated cytotoxicity on measles virus-infected cells
Rentier, Bernard ULg; Wallen, William C.

in Infection and Immunity (1980), 30(1), 303-315

The structural events related to antibody-dependent lymphocyte-mediated cytotoxicity (ADLC) have been studied on measles virus-infected cells using human peripheral blood lymphocytes (PBL) and anti ... [more ▼]

The structural events related to antibody-dependent lymphocyte-mediated cytotoxicity (ADLC) have been studied on measles virus-infected cells using human peripheral blood lymphocytes (PBL) and anti-measles virus serum. The first event in ADLC was a recognition process occurring within 15 min after contact between the infected cells and lymphocytes. Plasma membrane and microvilli of adsorbed PBL were specifically attached to virus-induced ridges over nucleocapsids and to viral buds. After 30 min, a fraction of adsorbed PBL (K cells) changed shape and extended long filipodia toward the target cells which, in turn, showed long villi contacting the PBL. At 4 h, when cytotoxicity as measured by chromium release was maximum, K cells had flattened and numerous blebs and ruffles formed on their surface. The K-cell alterations varied in intensity with the type of measles-infected target cell, but frequently the K cells appeared irreversibly damaged. T- and non-T-cell fractions were separated, and in situ erythrocyte rosettes were used as markers for subpopulations which were easily recognized by scanning electron microscopy. Most of the cytotoxic K cells were identified as non-T cells carrying Fc receptors for immunoglobulin G. However, a small subpopulation of cells bearing both sheep erythrocyte and Fc receptors was also found to be involved in ADLC by chromium release assay as well as by electron microscopy. Some of these interacting T cells extended a long uropod on the target cell, but their intracellular structure remained unaltered through ADLC, in contrast with the other T cells and the non-T killer cells. This suggests that perhaps some T killer cells might remain functional after the cytotoxic interaction with a target cell. [less ▲]

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See detailStructural studies of the surface of virus-infected cells
Dubois-Dalcq, Monique; Rentier, Bernard ULg

in Progress in Medical Virology (1980), 26

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See detailImprovements in ultrastructural localization of intracellular and membrane components of neurotropic viruses
Dubois-Dalcq, Monique; Rentier, Bernard ULg

in Brederoo, P.; De Priester, W. (Eds.) Electron microscopy, 1980 : proceedings of the Seventh European Congress on Electron Microscopy [Volume 2] (1980)

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See detailStructural study of adhesion and interaction of human lymphocytes and measles virus-infected cells during antibody dependent cellular cytotoxicity
Rentier, Bernard ULg

in Multiple Sclerosis Society (Ed.) Cellular aggregation and other membrane phenomena in multiple sclerosis (1980)

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See detailAttempt to isolate infectious agent from bone-marrow of patients with multiple sclerosis
Wallen, William C.; Sever, John L.; McFarlin, Dale E. et al

in Lancet (1979), 314(8139), 414-415

An infectious ætiology for multiple sclerosis (MS) has been postulated but none of the agents putatively associated with the disease have, as yet, been proven to be causative.1-4 The reported5 isolation ... [more ▼]

An infectious ætiology for multiple sclerosis (MS) has been postulated but none of the agents putatively associated with the disease have, as yet, been proven to be causative.1-4 The reported5 isolation of an infectious agent from bone-marrow aspiration of patients with MS prompted us to attempt recovery of an agent from our MS patients. We were unable to isolate an agent from seven MS patients with similar cell lines and procedures. There is no apparent reason for our inability to do so. However, we did find an adventitious agent(s) in two commercial sources of Hela cells. Although not initially apparent, this agent(s) became active upon incubation with either MS-patient or control bone-marrow cells and induced large syncytia when passed to other Hela cells. [less ▲]

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See detailParticipation in antibody dependent lymphocyte cytotoxicity of Fc bearing T lymphocytes
Wallen, W. C.; Rentier, Bernard ULg; Traub, R. G.

in Abstracts of the Annual Meeting of the American Society for Microbiology (1979)

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See detailElectron microscopic study of measles virus infection: unusual antibody-triggered redistribution of antigens on giant cells
Hooghe-Peters, Elisabeth L.; Rentier, Bernard ULg; Dubois-Dalcq, Monique

in Journal of Virology (1979), 29(2), 666-676

Vero cells infected with measles virus fuse to form multinucleated cells which incorporated virus- specific antigens in their membrane. The distribution of these antigens was analyzed after a brief ... [more ▼]

Vero cells infected with measles virus fuse to form multinucleated cells which incorporated virus- specific antigens in their membrane. The distribution of these antigens was analyzed after a brief treatment with human anti-measles immunoglobulin G, using autoradiography and immunoperoxidase labeling combined with transmission and scanning electron microscopy. Virus-specific antigens were distributed over the entire surface of giant cells treated at 4°C with human anti-measles immunoglobulin G and labeled Protein A. When cells were shifted to 37°C, labeled antigen-antibody complexes were redistributed in two stages. Patch formation occurred in 5 to 15 min. Later, antigen- antibody complexes became concentrated in a paracentral "ring" rather than typical caps. Patch formation occurred in the presence of metabolic inhibitors, whereas ring formation was inhibited by metabolic inhibitors. These rings contained membrane folds, villi, and viral buds, whereas the rest of the membrane was smooth. In addition, shedding, endocytosis of antigen-antibody complexes, and reexpression of antigens were observed. Antibodies to nonviral membrane antigens induced the same pattern of redistribution. Infected cells treated with anti-measles Fab' fragments maintained a homogeneous distribution of label throughout the experiments. In conclusion, intact immunoglobulins, but not Fab' fragments, were able to induce a dramatic redistribution of viral antigen on the membrane of giant cells infected with measles virus. [less ▲]

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See detailElectron microscopic study of measles virus infection: cell fusion and hemadsorption
Rentier, Bernard ULg; Hooghe-Peters, Elisabeth L.; Dubois-Dalcq, Monique

in Journal of Virology (1978), 28(2), 567-577

Virus-induced cell fusion has been studied after infection of Vero cells with measles virus. Scanning and transmission electron microscopy were combined with immunoperoxidase labeling of measles antigens ... [more ▼]

Virus-induced cell fusion has been studied after infection of Vero cells with measles virus. Scanning and transmission electron microscopy were combined with immunoperoxidase labeling of measles antigens to correlate viral production and distribution of virus-induced erythrocyte binding sites with progress of fusion-Release of infectious virus started before syncytia were detected and decreased while the number and size of syncytia were increasing. Most virions were seen budding from mononucleated cells or from the periphery of syncytia where cells were being recruited. Moving inward, the surfaces of syncytia were covered with numerous ridges containing viral antigen, but few viral buds were seen, suggesting that syncytia might be sites of defective viral formation. Hemadsorption occurred predominantly within the confines of syncytia. Erythrocytes were scattered sparsely over immature syncytia but were densely packed in the center of mature syncytia. Active binding sites for erythrocytes were located on cell villi and ridges covered with measles antigens. Hemadsorption was completely inhibited in measles virus-infected cultures pretreated with virus- specific immunoglobulin G for 1 h at 4°C. However, when these cultures were shifted to 37°C, hemadsorbing sites were recovered at the periphery of enlarging syncytia. Virus-induced sites for erythrocyte adsorption were found to move centripetally on syncytium membranes as fusion progressed. [less ▲]

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See detailStructural basis of hemadsorbing sites during the formation of syncytia in measles-infected cells
Rentier, Bernard ULg; Dubois-Dalcq, Monique

in Journal of Cell Biology (1977), 75

The surfaces of cells Infected with measles virus adsorb monkey red blood cells (RBC). In this study, the structure and localization of viral hemadsorbing (HAD) sites and their relationship with antigenic ... [more ▼]

The surfaces of cells Infected with measles virus adsorb monkey red blood cells (RBC). In this study, the structure and localization of viral hemadsorbing (HAD) sites and their relationship with antigenic sites and with cell fusion were investigated in measles virus infected Vero cells. Transmission and scanning electron microscopy were combined with immunolabeling, using human anti-measles IgG (Ab) and protein A from Staph, aureus coupled to peroxidase.. In the early syncytia (50-100 2 in diameter), HAD sites were clustered in the center but scattered at the periphery. In contrast, mature giant cells (400 to 500 2) had all HAD sites in the central area which displayed scattered villi. The periphery of the mature giant cells and the mononucleated cells did not hemadsorb but were covered with numerous villi. In the central area, RBC were firmly attached to villi and ridges over nucleocapsids but rarely to viral buds. Villi and ridges under the RBC were covered with antigenic sites which were not detected at the periphery of the mature syncytia. When living cells were treated with Ab at 4°C, complete inhibition of hemadsorption was only observed when RBC were applied to the cells in the cold. In other experiments, cells reacted with Ab at 4°C were washed, brought to 37°C and treated with RBC immediately or after 1-24 hrs. After 1-2 hrs, some HAD sites were present only at the periphery of immature giant cells, suggesting that RBC receptors had already emerged in membrane areas where fusion started again. After 24 hrs, the distribution of HAD and antigenic sites was the same as on cells not exposed to Ab. It seems that when fusion begins, HAD sites appeared on the periphery of the syncytia and then move spontaneously towards the center. With cessation of fusion, HAD sites disappear from the periphery of the giant cell. Receptors for RBC are closely associated with antigenic sites and correlated with viral induced fusion but not with virus production. [less ▲]

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