References of "Rogister, Bernard"
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See detailProteomic comparison of High and Low responders to eccentric exercise
Hody, Stéphanie ULg; Croisier, Jean-Louis ULg; Leprince, Pierre ULg et al

in Abstract book du Colloque de la Société Belge des Neurosciences (2009, May)

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See detailCourbatures après exercice excentrique : High et Low responders ?
Hody, Stéphanie ULg; Rogister, Bernard ULg; Croisier, Jean-Louis ULg et al

in Croisier, Jean-Louis; Codine, Philippe (Eds.) Exercice musculaire excentrique (2009)

It is well known that novel and/or unusual exercise consisting of lengthening muscle contractions (eccentric exercise) results in muscle damage. Muscle damage can be assessed via measures of indirect ... [more ▼]

It is well known that novel and/or unusual exercise consisting of lengthening muscle contractions (eccentric exercise) results in muscle damage. Muscle damage can be assessed via measures of indirect markers such as isometric strength, range of motion, blood levels of muscle-specific proteins and muscle soreness. It has been shown that changes in these markers present a large inter-subject variability. Especially, the seric CK response to exercise is largely documented and some authors introduced the notion of High and Low responders to define subjects with exaggerated and light or moderate response to eccentric protocol, respectively. The reasons for the various susceptibility to eccentric exercise are not understood but it seems to be influenced by several factors including genetical, morphological, physiological or training elements. Further studies are necessary to elucidate the underlying mechanisms of the large inter-subject variability in responses to eccentric exercise and in this context, a proteomic approach could be interesting to highlight protein expression differences between High and Low responders. [less ▲]

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See detailDOMS : traiter ou prévenir ?
Hody, Stéphanie ULg; Rogister, Bernard ULg; Leprince, Pierre ULg et al

in Croisier, Jean-Louis; Codine, Philippe (Eds.) Exercice musculaire excentrique (2009)

The evidence of benefits from eccentric contraction provides compelling rationale for their inclusion in force training and in the reeducation of various locomotor pathologies (i.e., tendinopathies or ... [more ▼]

The evidence of benefits from eccentric contraction provides compelling rationale for their inclusion in force training and in the reeducation of various locomotor pathologies (i.e., tendinopathies or muscular imbalance). However, intense or unusual eccentric exercise frequently leads to muscle damage associated with prolonged loss in muscle strength and range of motion, a dramatic increase in muscle proteins circulating in blood and the development of muscle soreness. These negative functional consequences, referred to as Delayed Onset Muscle Soreness (DOMS), often disturb the progress of training or reeducation programmes. In an attempt to attenuate signs and symptoms of DOMS, several approaches have been used prophylactically and/or therapeutically. This article focuses on some of the most commonly used modalities, including the nutritionnal and pharmacological strategies, clinical therapies and exercise. Despite a large number of studies, there is little evidence indicating any benefit at the perfomance level of these various approaches. Conversely, there is unequivocal evidence that a bout of eccentric exercise is followed by protection against skeletal muscle damage associated with a subsequent bout of potentially damaging exercise for several weeks to several months. To date, specific submaximal training appears the most efficient prophylactic measure and is recommended to alleviate the prejudiciable consequences associated with DOMS in the athletic or therapeutic programs. Despite the volume of data concerning this protective effect, often called the “repeated bout effect”, the underlying mechanisms of such an adaptation are not fully understood and a better knowledge of these adaptative mechanisms could provide better guidelines for prevention or treatment practice. [less ▲]

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See detailLa neurogenese adulte ou l'histoire d'un dogme qui s'ecroule.
Pirotte, Dorothée ULg; Rogister, Bernard ULg

in Revue Médicale de Liège (2008), 63(5-6), 245-50

The history of sciences is characterized by major discoveries, but also by challenges of theories or dogma previously established and accepted by everybody. One of the recent examples illustrating such a ... [more ▼]

The history of sciences is characterized by major discoveries, but also by challenges of theories or dogma previously established and accepted by everybody. One of the recent examples illustrating such a questioning relates to the demonstration of the persistence of a cerebral neurogenesis in the adult brain, including in human. This adult neurogenesis is however limited, both in space (it concerns only the subventricular zone and the gyrus dentatus in the hippocampus) and the type of newly-formed neurons (interneurones which most of them are GABAergic and present respectively in the olfactive bulb and CA1 area of the hippocampus). Moreover, this neurogenesis does not seem to be recruited after a brain lesion, a situation which explains why functional recovery when it is observed remains a consequence of brain plasticity. We thus legitimately address the question about the physiological role of this adult brain neurogenesis as well as a possible implication in the aetiology of various neurological disorders, like the neurodegenerative diseases or epilepsy, but also in psychiatric diseases like depression. [less ▲]

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See detailLes glioblastomes, un exemple de recherche translationnelle?
Kroonen, Jérôme ULg; Nguyen-Khac, Minh-Tuan ULg; Deprez, Manuel ULg et al

in Revue Médicale de Liège (2008), 63(5-6), 251-6

Among patients which develop glioblastoma multiform (GBM), recurrence is the rule despite continuous progress in surgery, radiotherapy and chemotherapy. In the adult, GBM is the most frequent and most ... [more ▼]

Among patients which develop glioblastoma multiform (GBM), recurrence is the rule despite continuous progress in surgery, radiotherapy and chemotherapy. In the adult, GBM is the most frequent and most aggressive tumour of the Central Nervous System. A better understanding of the mechanisms by which these tumours relapse could promote the use of preventive therapy and could increase patients' survival. GBM stem cells have been recently described and it was demonstrated that they are specifically implied in the experimental tumorigenesis. It is thus very attractive to speculate on a possible relationship between these GBM stem cells and the neural stem cells which are persisting in the neurogenic zones of the adult brain. In this review, we formulate and discuss the hypothesis by which, in a patient with GBM, malignant stem cells might be present in the neurogenic zones, away from the tumour mass. This hypothesis could explain the tumour relapse observed after the first treatments. [less ▲]

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See detailStem cell factor and mesenchymal and neural stem cell transplantation in a rat model of Huntington's disease.
Bantubungi, Kadiombo; Blum, David; Cuvelier, Laetitia et al

in Molecular & Cellular Neuroscience [=MCN] (2008), 37(3), 454-70

Neural and mesenchymal stem cells have been proposed as alternative sources of cells for transplantation into the brain in neurodegenerative disorders. However, the endogenous factors controlling their ... [more ▼]

Neural and mesenchymal stem cells have been proposed as alternative sources of cells for transplantation into the brain in neurodegenerative disorders. However, the endogenous factors controlling their engraftment within the injured parenchyma remain ill-defined. Here, we demonstrate significant engraftment of undifferentiated exogenous mesenchymal or neural stem cells throughout the lesioned area in a rat model for Huntington's disease, as late as 8 weeks post-transplantation. We show that stem cell factor (SCF), strongly up-regulated within host cells in the damaged striatum, is able to activate the SCF receptor c-kit and its signaling pathway and to promote the migration and proliferation of mesenchymal and neural stem cells in vitro. Furthermore, c-kit receptor blockade alters neural stem cell distribution within the lesioned striatum. Host SCF expression is observed in atypical cells expressing glial fibrillary acidic protein and doublecortin in the lesioned striatum and in migrating doublecortin-positive progenitors. Taken together, these data demonstrate that SCF produced in situ in the lesioned striatum is an important factor in promoting the engraftment of stem cells within the lesioned brain. [less ▲]

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See detailInterest of a comparative proteomic approach to unravel the aetiology of DOMS in humans
Hody, Stéphanie ULg; Croisier, Jean-Louis ULg; Wang, François-Charles ULg et al

in Acta Physiologica Scandinavica. Supplementum (2008), 194(suppl 666), -09

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See detailDoes neural phenotypic plasticity from non-neural cells really exist?
Wislet, Sabine ULg; wautier, Franz; Laudet, Emerence ULg et al

in Ivanova, laura (Ed.) Cell differentiation Research Developments (2008)

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See detailInterest of a comparative proteomic approach to unravel the aetiology of DOMS in humans
Hody, Stéphanie ULg; Croisier, Jean-Louis ULg; WANG, François-Charles ULg et al

in Abstract Book of Proteom’ Lux 2007 (2007, October)

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See detailSufasalazine unveils a contact-independent HSV-TK/ganciclovir gene therapy bystander effect in malignant gliomas
Robe, Pierre ULg; Nguyen-Khac, Minh-Tuan ULg; Lambert, Frédéric ULg et al

in International Journal of Oncology (2007), 30(1), 283-290

The efficacy of HSV-TK/ganciclovir-based gene therapy on malignant gliomas largely relies on the amplitude of the bystander effect. In these experiments, the anti-inflammatory drug Sulfasalazine increased ... [more ▼]

The efficacy of HSV-TK/ganciclovir-based gene therapy on malignant gliomas largely relies on the amplitude of the bystander effect. In these experiments, the anti-inflammatory drug Sulfasalazine increased the HSV-TK/ganciclovir bystander effect in C6, 9L and LN18 cells but not in U87 glioma cells. Using bi-compartmental culture devices and conditioned medium transfer experiments, we showed that in C6, 9L and LN18 cells but not in U87 cells, Sulfasalazine also unveiled a new, contact-independent mechanism of HSV-TK/ganciclovir bystander effect. Upon treatment with ganciclovir, human LN18-TK but not U87-TK cells synthetized and released TNF-alpha in the culture medium. Sulfasalazine sensitized glioma cells to the toxic effect of TNF-alpha. and enhanced its secretion in LN18-TK cells in response to GCV treatment. The caspase-8 inhibitor Z-IETD-FMK and a blocking antibody to TNF-alpha both inhibited the contact-independent bystander effect in LN18 cells. Taken together, these results suggest that TNF-alpha mediates the contact-independent bystander effect in LN18 cells. The treatment with GCV and/or Sulfasalazine of tumor xenografts consisting of a mix of 98% C6 and 2% C6-TK cells shows that Sulfasalazine is also a potent adjunct to the in vivo treatment of gliomas. [less ▲]

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See detailRegulation of nestin expression by thrombin and cell density in cultures of bone mesenchymal stem cells and radial glial cells.
Wislet-Gendebien, Sabine ULg; wautier, Franz; Chanas, Grazyna et al

in BMC Neuroscience (2007), 8

BACKGROUND: Bone marrow stromal cells and radial glia are two stem cell types with neural phenotypic plasticity. Bone marrow mesenchymal stem cells can differentiate into osteocytes, chondrocytes and ... [more ▼]

BACKGROUND: Bone marrow stromal cells and radial glia are two stem cell types with neural phenotypic plasticity. Bone marrow mesenchymal stem cells can differentiate into osteocytes, chondrocytes and adipocytes, but can also differentiate into non-mesenchymal cell, i.e. neural cells in appropriate in vivo and in vitro experimental conditions. Likewise, radial glial cells are the progenitors of many neurons in the developing cortex, but can also generate astrocytes. Both cell types express nestin, an intermediate filament protein which is the hallmark of neural precursors. RESULTS: In this study, we demonstrate that thrombin, a multifunctional serine protease, stimulates the growth of radial glial cells (RG) and mesenchymal stem cells (MSCs) in a dose-dependent manner. In RG, the mitogenic effect of thrombin is correlated with increased expression of nestin but in MSCs, this mitogenic effect is associated with nestin down-regulation. Both cell types express the PAR-1 type receptor for Thrombin and the effect of Thrombin on both cell types can be mimicked by its analogue TRAP-6 activating specifically this receptor subtype or by serum which contains various amount of thrombin. Moreover, we also demonstrate that serum deprivation-induced expression of nestin in MSCs is inhibited by high cell density (> 50,000 cells/cm2). CONCLUSION: This work shows that thrombin stimulates the growth of both RG and MSCs and that nestin expression by MSCs and RG is regulated in opposite manner by thrombin in vitro. Thrombin effect is thus associated in both cell types with a proliferating, undifferentiated state but in RG this involves the induction of nestin expression, a marker of immaturity for neural progenitors. In MSCs however, nestin expression, as it corresponds to a progression from the mesenchymal "undifferentiated", proliferating phenotype toward acquisition of a neural fate, is inhibited by the mitogenic signal. [less ▲]

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See detailTranscriptional regulation of the mouse doublecortin gene in differentiating neurons
Plumier, Jean-Christophe ULg; Muller, Marc ULg; Rogister, Bernard ULg et al

in International Journal of Developmental Neuroscience (2006, December), 24(8), 535

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See detailTranscription impairment and cell migration defects in elongator-depleted cells: Implication for familial dysautonomia
Close, Pierre ULg; Hawkes, Nicola; Cornez, Isabelle ULg et al

in Molecular Cell (2006), 22(4), 521-531

Mutations in IKBKAP, encoding a subunit of Elongator, cause familial dysautonomia (FD), a severe neuro-developmental disease with complex clinical characteristics. Elongator was previously linked not only ... [more ▼]

Mutations in IKBKAP, encoding a subunit of Elongator, cause familial dysautonomia (FD), a severe neuro-developmental disease with complex clinical characteristics. Elongator was previously linked not only with transcriptional elongation and histone acetylation but also with other cellular processes. Here, we used RNA interference (RNAi) and fibroblasts from FD patients to identify Elongator target genes and study the role of Elongator in transcription. Strikingly, whereas Elongator is recruited to both target and nontarget genes, only target genes display histone H3 hypoacetylation and progressively lower RNAPII density through the coding region in FD cells. Interestingly, several target genes encode proteins implicated in cell motility. Indeed, characterization of IKAP/hELP1 RNAi cells, FD fibroblasts, and neuronal cell-derived cells uncovered defects in this cellular function upon Elongator depletion. These results indicate that defects in Elongator function affect transcriptional elongation of several genes and that the ensuing cell motility deficiencies may underlie the neuropathology of FD patients. [less ▲]

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See detailTranscriptional regulation of the mouse doublecortin gene in differentiating neurons
Plumier, Jean-Christophe ULg; Muller, Marc ULg; Rogister, Bernard ULg et al

in International Journal of Developmental Neuroscience (2006), 24

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See detailDevelopmental regulation of beta-carboline-induced inhibition of glycine-evoked responses depends on glycine receptor beta subunit expression
Mangin, Jean-Marie; Nguyen, Laurent ULg; Gougnard, Catherine et al

in Molecular Pharmacology (2005), 67(5), 1783-1796

In this work, we show that beta-carbolines, which are known negative allosteric modulators of GABA A receptors, inhibit glycine-induced currents of embryonic mouse spinal cord and hippocampal neurons. In ... [more ▼]

In this work, we show that beta-carbolines, which are known negative allosteric modulators of GABA A receptors, inhibit glycine-induced currents of embryonic mouse spinal cord and hippocampal neurons. In both cell types, beta-carboline-induced inhibition of glycine receptor (GlyR)-mediated responses decreases with time in culture. Single-channel recordings show that the major conductance levels of GlyR unitary currents shifts from high levels (>= 50 pS) in 2 to 3 days in vitro (DIV) neurons to low levels (< 50 pS) in 11 to 14 DIV neurons, assessing the replacement of functional homomeric GlyR by heteromeric GlyR. In cultured spinal cord neurons, the disappearance of beta-carboline inhibition of glycine responses and high conductance levels is almost complete in mature neurons, whereas a weaker decrease in beta-carboline-evoked glycine response inhibition and high conductance level proportion is observed in hippocampal neurons. To confirm the hypothesis that the decreased sensitivity of GlyR to beta-carbolines depends on beta subunit expression, Chinese hamster ovary cells were permanently transfected either with GlyR alpha 2 subunit alone or in combination with GlyR beta subunit. Single-channel recordings revealed that the major conductance levels shifted from high levels (>= 50 pS) in GlyR-alpha 2-transfected cells to low levels (< 50 pS) in GlyR-alpha 2-containing cells. Consistently, both picrotoxinand beta-carboline-induced inhibition of glycine-gated currents were significantly decreased in GlyR-alpha 2-transfected cells compared with GlyR-alpha 2-containing cells. In summary, we demonstrate that the incorporation of beta subunits in GlyRs confers resistance not only to picrotoxin but also to beta-carbolineinduced inhibition. Furthermore, we also provide evidence that hippocampal neurons undergo in vitro a partial maturation process of their GlyR-mediated responses. [less ▲]

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See detailPeripheral benzodiazepine receptor (PBR) ligand cytotoxicity unrelated to PBR expression
Hans, Grégory ULg; Wislet, Sabine ULg; Lallemend, François et al

in Biochemical Pharmacology (2005), 69(5), 819-830

Some synthetic ligands of the peripheral-type benzodiazepine receptor (PBR), an 18 kDa protein of the outer mitochondrial membrane, are cytotoxic for several tumor cell lines and arise as promising ... [more ▼]

Some synthetic ligands of the peripheral-type benzodiazepine receptor (PBR), an 18 kDa protein of the outer mitochondrial membrane, are cytotoxic for several tumor cell lines and arise as promising chemotherapeutic candidates. However, conflicting results were reported regarding the actual effect of these drugs on cellular survival ranging from protection to toxicity. Moreover, the concentrations needed to observe such a toxicity were usually high, far above the affinity range for their receptor, hence questioning its specificity. In the present study, we have shown that micromolar concentrations of FGIN-1-27 And Ro 5-4864, two chemically unrelated PBR ligands are toxic for both PBR-expressing SK-N-BE neuroblastoma cells and PBR-deficient Jurkat lymphoma cells. We have thereby demonstrated that the cytotoxicity of these drugs is unrelated to their PBR-binding activity. Moreover, Ro 54864-induced cell death differed strikingly between both cell types, being apoptotic in Jurkat cells while necrotic in SK-N-BE cells. Again, this did not seem to be related to PBR expression since Ro 5-4864-induced death of PBR-transfected Jurkat cells remained apoptotic. Taken together, our results show that PBR is unlikely to mediate all the effects of these PBR ligands. They however confirm that some of these ligands are very effective cytotoxic drugs towards various cancer cells, even for reputed chemoresistant tumors such as neuroblastoma, and, surprisingly, also for PBR-lacking tumor cells. (C) 2004 Elsevier Inc. All rights reserved. [less ▲]

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See detailbeta-carbolines induce apoptosis in cultured cerebellar granule neurons via the mitochondrial pathway
Hans, Grégory ULg; Malgrange, Brigitte ULg; Lallemend, François et al

in Neuropharmacology (2005), 48(1), 105-117

N-Butyl-beta-carboline-3-carboxylate (betaCCB) is, together with 2-methyl-norharmanium and 2,9-dimethylnorharmanium ions, an endogenously occurring beta-carboline. Due to their structural similarities ... [more ▼]

N-Butyl-beta-carboline-3-carboxylate (betaCCB) is, together with 2-methyl-norharmanium and 2,9-dimethylnorharmanium ions, an endogenously occurring beta-carboline. Due to their structural similarities with the synthetic neurotoxin 1-methy14-phenyl-1,2,3,6-tetrahydropyridine (MPTP), harman and norharman compounds have been proposed to be involved in the pathogenesis of Parkinson's disease. While also structurally related, betaCCB has received much less interest in that respect although we had previously demonstrated that it induces the apoptotic cell death of cultured cerebellar granule neurons (CGNs). Herein, we have investigated the molecular events leading to CGN apoptosis upon betaCCB treatment. We first demonstrated that betaCCB-induced apoptosis occurs in neurons only, most likely as a consequence of a specific neuronal uptake as shown using binding/uptake experiments. Then we observed that, in betaCCB-treated CGNs, caspases 9, 3 and 8 were successively activated, suegesing an activation of the mitochondrial pathway. Consistently, betaCCB also induced the release from the mitochondrial intermembrane space of two pro-apoptotic factors. i.e. cytochrome c and apotptosis inducing factor (AIF). Interestingly, no mitochondrial membrane depolarisation was associated with this release. suggesting a mitochondrial permeability transition pore-independent mechanism. The absence of any neuroprotective effect provided by two mPTP inhibitors. i.e. cyclosporine A and bongkrekic acid. further supported this hypothesis. Together. these results show that betaCCB is specifically taken up by neuronal cells where it triggers a specific permeabilization of the outer mitochondrial membrane and a subsequent apoptotic cell death. (C) 2004 Elsevier Ltd. All rights reserved. [less ▲]

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