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See detailComplex invasion pattern of the cerebral cortex bymicroglial cells during development of the mouse embryo.
Avila Macaya, Ariel Salvatore ULg

in Glia (2012)

Microglia are the immune cells of the central nervous system. They are suspected to play important roles in adult synaptogenesis and in the development of the neuronal network. Microglial cells originate ... [more ▼]

Microglia are the immune cells of the central nervous system. They are suspected to play important roles in adult synaptogenesis and in the development of the neuronal network. Microglial cells originate from progenitors in the yolk sac. Although it was suggested that they invade the cortex at early developmental stages in the embryo, their invasion pattern remains largely unknown. To address this issue we analyzed the pattern of cortical invasion by microglial cells in mouse embryos at the onset of neuronal cell migration using in vivo immunohistochemistry and ex vivo time-lapse analysis of microglial cells. Microglial cells begin to invade the cortex at 11.5 days of embryonic age (E11.5). They first accumulate at the pial surface and within the lateral ventricles, after which they spread throughout the cortical wall, avoiding the cortical plate region in later embryonic ages. The invasion of the cortical parenchyma occurs in different phases. First, there is a gradual increase of microglial cells between E10.5 and E14.5. From E14.5 to E15.5 there is a rapid phase with a massive increase in microglia, followed by a slow phase again from E15.5 until E17.5. At early stages, many peripheral microglia are actively proliferating before entering the parenchyma. Remarkably, activated microglia accumulate in the choroid plexus primordium, where they are in the proximity of dying cells. Time-lapse analysis shows that embryonic microglia are highly dynamic cells. [less ▲]

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See detailInvolvement of placental growth factor in Wallerian degeneration
Chaballe, Linda ULg; Close, Pierre ULg; SEMPELS, Maxime ULg et al

in Glia (2011), 59(3), 379-396

Wallerian degeneration (WD) is an inflammatory process of nerve degeneration, which occurs more rapidly in the peripheral nervous system compared with the central nervous system, resulting, respectively ... [more ▼]

Wallerian degeneration (WD) is an inflammatory process of nerve degeneration, which occurs more rapidly in the peripheral nervous system compared with the central nervous system, resulting, respectively in successful and aborted axon regeneration. In the peripheral nervous system, Schwann cells (SCs) and macrophages, under the control of a network of cytokines and chemokines, represent the main cell types involved in this process. Within this network, the role of placental growth factor (PlGF) remains totally unknown. However, properties like monocyte activation/attraction, ability to increase expression of pro-inflammatory molecules, as well as neuroprotective effects, make it a candidate likely implicated in this process. Also, nothing is described about the expression and localization of this molecule in the peripheral nervous system. To address these original questions, we decided to study PlGF expression under physiological and degenerative conditions and to explore its role in WD, using a model of sciatic nerve transection in wild-type and Pgf(-/-) mice. Our data show dynamic changes of PlGF expression, from periaxonal in normal nerve to SCs 24h postinjury, in parallel with a p65/NF-κB recruitment on Pgf promoter. After injury, SC proliferation is reduced by 30% in absence of PlGF. Macrophage invasion is significantly delayed in Pgf(-/-) mice compared with wild-type mice, which results in worse functional recovery. MCP-1 and proMMP-9 exhibit a 3-fold reduction of their relative expressions in Pgf(-/-) injured nerves, as demonstrated by cytokine array. In conclusion, this work originally describes PlGF as a novel member of the cytokine network of WD. [less ▲]

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See detailShaker-type potassium channel subunits differentially control oligodendrocyte progenitor proliferation
Vautier, Francois; Belachew, Shibeshih ULg; Chittajallu, Ramesh et al

in Glia (2004), 48(4), 337-345

Oligodendrocyte precursor (OP) cells are exposed to multiple extrinsic signals that control their proliferation and differentiation. Previous cell proliferation studies and electrophysiological analysis ... [more ▼]

Oligodendrocyte precursor (OP) cells are exposed to multiple extrinsic signals that control their proliferation and differentiation. Previous cell proliferation studies and electrophysiological analysis in cultured cells and in brain slices have suggested that outward potassium channels, particularly Kv1 subunits, may have a prominent role in OP cell proliferation. In the present study, we assessed to what extent overexpression of Kv1.3, Kv1.4, Kv1.5, and Kv1.6 can affect OP cell proliferation and differentiation in culture. We observed that overexpression of Kv1.3 or Kv1.4 increased OP cell proliferation in the absence of mitogens, whereas Kv1.6 overexpression inhibited mitogen-induced OP cell cycle progression. Interestingly, Kv1.3, Kv1.4, Kv1.5, and Kv1.6 overexpression did not interfere with the kinetics of oligodendrocyte differentiation. This study represents the first demonstration that the activity of potassium channels containing distinct Kv1 subunit proteins directly controls oligodendroglial proliferation in the presence of mitogens, as well as in growth factor-free conditions. (C) 2004 Wiley-Liss, Inc. [less ▲]

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See detailSynaptic and extrasynaptic neurotransmitter receptors in glial precursors' quest for identity
Belachew, Shibeshih ULg; Gallo, Vittorio

in Glia (2004), 48(3), 185-196

It is widely established that neurotransmitter receptors are expressed in non-neuronal cells, and particularly in neural progenitor cells in the postnatal central nervous system. The functional role of ... [more ▼]

It is widely established that neurotransmitter receptors are expressed in non-neuronal cells, and particularly in neural progenitor cells in the postnatal central nervous system. The functional role of these receptors during development is unclear, but it needs to be revisited now that cells previously considered restricted to glial lineages have been shown to generate neurons. The present review integrates recent advances, to shed new light on how neurotransmitter receptors may, alternatively, serve as excitable mediators of neuron-glia and neuron-neuroblast interactions. (C) 2004 Wiley-Liss, Inc. [less ▲]

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See detailNestin expression in cultivated mesenchymal stem cells: Regulation and potential role in their neural differentiation
Wislet-Gendebien, Sabine ULg; Leprince, Pierre ULg; Moonen, Gustave ULg et al

in Glia (2002, May), (Suppl. 1), 87

Bone marrow stromal cells can differentiate into many types of mesenchymal cells, i.e. osteocyte, chondrocyte, fibroblast and adipocyte, but can also differentiate into non-mesenchymal cell, i.e. neural ... [more ▼]

Bone marrow stromal cells can differentiate into many types of mesenchymal cells, i.e. osteocyte, chondrocyte, fibroblast and adipocyte, but can also differentiate into non-mesenchymal cell, i.e. neural cells in appropriate in vivo experimental conditions (Kopen and al.,PNAS,96, 10711,1999, Brazelton and al, Science, 290,1175, 2000, Mezey and al, Science, 290,1179, 2000). In neurological disorders, such as Alzheimer's and Parkinson's diseases, auto-transplantation of neural cell types derived from mesenchymal stem cells offers the potential of replacing lost cells and recovering lost functions. Nestin is an intermediate filament protein predominantly expressed by neural stem cells and is used to identify neural progenitor. In this study, we demonstrate that cultured rat mesenchymal stem cells (rMSC) can express nestin in appropriate conditions. Two factors contribute to the regulation of nestin expression by rMSC : 1) the presence of serum-derived components in the culture medium which repress nestin expression and 2) the cell’s number of passages. LPA and thrombin mimic this serum effect. Furthermore, when nestin- positive cells are trypsinized and resuspended into culture conditions used for neural stem cells (NSC), sphere formation is observed. Likewise, by co-cultivating nestin-positive rMSC with NSC derived from green mouse, heterogenous spheres were obtained. When those heterogenous spheres are placed on polyornithine-coated surfaces, a differentiation of some rMSC into GFAP-positive cells occurs. These results indicate that nestin expression might be a pre-requisite for the acquisition by rMSC of the capacity to differentiate into some neural cell types. [less ▲]

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See detailRhoA inhibition is a key step in pituicyte stellation induced by A(1)-type adenosine receptor activation.
Rosso, Lia; Peteri-Brunback, Brigitta; Vouret-Craviari, Valerie et al

in Glia (2002), 38(4), 351-62

Pituicyte stellation in vitro represents a useful model with which to study morphological changes that occur in vivo in these cells during times of high neurohypophysial hormone output. This model has ... [more ▼]

Pituicyte stellation in vitro represents a useful model with which to study morphological changes that occur in vivo in these cells during times of high neurohypophysial hormone output. This model has helped us establish the hypothesis of a purinergic regulation of pituicyte morphological plasticity. We first show that ATP induces stellation in 37% of pituicytes, an effect that is secondary to the metabolism of ATP to adenosine. Adenosine-induced stellation of pituicytes appears to be mediated by A(1)-type receptors. The effect is independent of intracellular calcium and does not involve the mitogen-activated protein kinase pathway. The basal (nonstellate) state of pituicytes depends on tonic activation of a Rho GTPase because both C3 transferase (a Rho inhibitor) and Y-27632 (an inhibitor of p160Rho kinase) can induce stellation. Lysophosphatidic acid, a Rho activator, blocks the morphogenic effect of adenosine dose-dependently. Using a specific RhoA pull-down assay, we also show that downregulation of activated RhoA is the key event coupling A(1) receptor activation to pituicyte stellation, via F-actin depolymerization and microtubule reorganization. Finally, both vasopressin and oxytocin can prevent or reverse adenosine-induced stellation. The effects of vasopressin, and those of high concentrations of oxytocin, are mediated through V(1a) receptors. Placed within the context of the relevant literature, our data suggest the possibility of a purinergic regulation of pituicyte morphological plasticity and subsequent modulation of hormone release, with these hormones providing a negative feedback mechanism. [less ▲]

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See detailontogeny of radial and other astroglial cells in murine cerebral cortex
Misson, Jean-Paul ULg; takahashi, takao; caviness, verne S

in Glia (1991), 4

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See detailOntogeny of radial and other astroglial cells in murine cerebral cortex
Misson, Jean-Paul ULg; Takahashi, Takao; Caviness, V. S.

in Glia (1991), 4

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See detailEnhanced Release of Plasminogen Activator Inhibitor(S) but Not of Plasminogen Activators by Cultured Rat Glial Cells Treated with Interleukin-1
Rogister, Bernard ULg; Leprince, Pierre ULg; Delree, P. et al

in Glia (1990), 3(4), 252-7

Astroglial cells are known to proliferate during development of the nervous system, as well as during post-traumatic gliosis. We have previously shown that the proliferation of cultured astrocytes can be ... [more ▼]

Astroglial cells are known to proliferate during development of the nervous system, as well as during post-traumatic gliosis. We have previously shown that the proliferation of cultured astrocytes can be stimulated by the urokinase-type (uPA) of plasminogen activator (PA) and that astrocytes are able to release such uPA upon stimulation with basic fibroblast growth factor, which is known to act as a mitogen for these cells. Here we report studies on the effects of human interleukin-1 (IL-1) on the release of PA activity by cultured newborn rat astroglial cells. Whereas there is controversy in the literature as to whether IL-1 stimulates multiplication of astroglial cells, we failed to observe such an effect in our system. We did observe, however, a dose-dependent decrease in PA activity in the supernatant of the IL-1 treated cultures. Further analysis revealed that this apparent decrease in PA release was in fact due to an increased release of plasminogen activator inhibitor (PAI). A similar IL-1 induced increase in PAI release was also found to occur in cultures of transformed astrocytes (human glioma LN18) and in cultured Schwann cells, but not in cultures of neurons or neuronal tumour cells. Since protease inhibitors are known to possess neuritogenic properties, our results suggest that IL-1, by its capacity to induce PAI, may promote neuritogenesis. [less ▲]

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