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  1. Article ; Online: Re-Evaluating the Relevance of the Oxygen-Glucose Deprivation Model in Ischemic Stroke: The Example of Cdk Inhibition.

    D'aes, Tine / Marlier, Quentin / Verteneuil, Sébastien / Quatresooz, Pascale / Vandenbosch, Renaud / Malgrange, Brigitte

    International journal of molecular sciences

    2023  Volume 24, Issue 8

    Abstract: Previous research has shown that cyclin-dependent kinases (Cdks) that play physiological roles in cell cycle regulation become activated in post-mitotic neurons after ischemic stroke, resulting in apoptotic neuronal death. In this article, we report our ... ...

    Abstract Previous research has shown that cyclin-dependent kinases (Cdks) that play physiological roles in cell cycle regulation become activated in post-mitotic neurons after ischemic stroke, resulting in apoptotic neuronal death. In this article, we report our results using the widely used oxygen-glucose deprivation (OGD) in vitro model of ischemic stroke on primary mouse cortical neurons to investigate whether Cdk7, as part of the Cdk-activating kinase (CAK) complex that activates cell cycle Cdks, might be a regulator of ischemic neuronal death and may potentially constitute a therapeutic target for neuroprotection. We found no evidence of neuroprotection with either pharmacological or genetic invalidation of Cdk7. Despite the well-established idea that apoptosis contributes to cell death in the ischemic penumbra, we also found no evidence of apoptosis in the OGD model. This could explain the absence of neuroprotection following Cdk7 invalidation in this model. Neurons exposed to OGD seem predisposed to die in an NMDA receptor-dependent manner that could not be prevented further downstream. Given the direct exposure of neurons to anoxia or severe hypoxia, it is questionable how relevant OGD is for modeling the ischemic penumbra. Due to remaining uncertainties about cell death after OGD, caution is warranted when using this in vitro model to identify new stroke therapies.
    MeSH term(s) Mice ; Animals ; Oxygen/metabolism ; Ischemic Stroke ; Glucose/metabolism ; Apoptosis/genetics ; Cell Death/physiology ; Hypoxia ; Cyclin-Dependent Kinases ; Cells, Cultured
    Chemical Substances Oxygen (S88TT14065) ; Glucose (IY9XDZ35W2) ; Cyclin-Dependent Kinases (EC 2.7.11.22)
    Language English
    Publishing date 2023-04-10
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms24087009
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Re-Evaluating the Relevance of the Oxygen–Glucose Deprivation Model in Ischemic Stroke

    Tine D’aes / Quentin Marlier / Sébastien Verteneuil / Pascale Quatresooz / Renaud Vandenbosch / Brigitte Malgrange

    International Journal of Molecular Sciences, Vol 24, Iss 7009, p

    The Example of Cdk Inhibition

    2023  Volume 7009

    Abstract: Previous research has shown that cyclin-dependent kinases (Cdks) that play physiological roles in cell cycle regulation become activated in post-mitotic neurons after ischemic stroke, resulting in apoptotic neuronal death. In this article, we report our ... ...

    Abstract Previous research has shown that cyclin-dependent kinases (Cdks) that play physiological roles in cell cycle regulation become activated in post-mitotic neurons after ischemic stroke, resulting in apoptotic neuronal death. In this article, we report our results using the widely used oxygen–glucose deprivation (OGD) in vitro model of ischemic stroke on primary mouse cortical neurons to investigate whether Cdk7, as part of the Cdk-activating kinase (CAK) complex that activates cell cycle Cdks, might be a regulator of ischemic neuronal death and may potentially constitute a therapeutic target for neuroprotection. We found no evidence of neuroprotection with either pharmacological or genetic invalidation of Cdk7. Despite the well-established idea that apoptosis contributes to cell death in the ischemic penumbra, we also found no evidence of apoptosis in the OGD model. This could explain the absence of neuroprotection following Cdk7 invalidation in this model. Neurons exposed to OGD seem predisposed to die in an NMDA receptor-dependent manner that could not be prevented further downstream. Given the direct exposure of neurons to anoxia or severe hypoxia, it is questionable how relevant OGD is for modeling the ischemic penumbra. Due to remaining uncertainties about cell death after OGD, caution is warranted when using this in vitro model to identify new stroke therapies.
    Keywords neurons ; cell culture ; OGD ; cortex ; mouse ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 571
    Language English
    Publishing date 2023-04-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article: Core cell cycle machinery is crucially involved in both life and death of post-mitotic neurons

    Marlier, Quentin / D’aes, Tine / Verteneuil, Sébastien / Vandenbosch, Renaud / Malgrange, Brigitte

    Cellular and molecular life sciences. 2020 Nov., v. 77, no. 22

    2020  

    Abstract: A persistent dogma in neuroscience supported the idea that terminally differentiated neurons permanently withdraw from the cell cycle. However, since the late 1990s, several studies have shown that cell cycle proteins are expressed in post-mitotic ... ...

    Abstract A persistent dogma in neuroscience supported the idea that terminally differentiated neurons permanently withdraw from the cell cycle. However, since the late 1990s, several studies have shown that cell cycle proteins are expressed in post-mitotic neurons under physiological conditions, indicating that the cell cycle machinery is not restricted to proliferating cells. Moreover, many studies have highlighted a clear link between cell cycle-related proteins and neurological disorders, particularly relating to apoptosis-induced neuronal death. Indeed, cell cycle-related proteins can be upregulated or overactivated in post-mitotic neurons in case of acute or degenerative central nervous system disease. Given the considerable lack of effective treatments for age-related neurological disorders, new therapeutic approaches targeting the cell cycle machinery might thus be considered. This review aims at summarizing current knowledge about the role of the cell cycle machinery in post-mitotic neurons in healthy and pathological conditions.
    Keywords cell cycle ; central nervous system ; death ; nervous system diseases ; neurons ; neurophysiology ; therapeutics
    Language English
    Dates of publication 2020-11
    Size p. 4553-4571.
    Publishing place Springer International Publishing
    Document type Article
    Note NAL-AP-2-clean ; Review
    ZDB-ID 1358415-7
    ISSN 1420-9071 ; 1420-682X
    ISSN (online) 1420-9071
    ISSN 1420-682X
    DOI 10.1007/s00018-020-03548-1
    Database NAL-Catalogue (AGRICOLA)

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  4. Article ; Online: Core cell cycle machinery is crucially involved in both life and death of post-mitotic neurons.

    Marlier, Quentin / D'aes, Tine / Verteneuil, Sébastien / Vandenbosch, Renaud / Malgrange, Brigitte

    Cellular and molecular life sciences : CMLS

    2020  Volume 77, Issue 22, Page(s) 4553–4571

    Abstract: A persistent dogma in neuroscience supported the idea that terminally differentiated neurons permanently withdraw from the cell cycle. However, since the late 1990s, several studies have shown that cell cycle proteins are expressed in post-mitotic ... ...

    Abstract A persistent dogma in neuroscience supported the idea that terminally differentiated neurons permanently withdraw from the cell cycle. However, since the late 1990s, several studies have shown that cell cycle proteins are expressed in post-mitotic neurons under physiological conditions, indicating that the cell cycle machinery is not restricted to proliferating cells. Moreover, many studies have highlighted a clear link between cell cycle-related proteins and neurological disorders, particularly relating to apoptosis-induced neuronal death. Indeed, cell cycle-related proteins can be upregulated or overactivated in post-mitotic neurons in case of acute or degenerative central nervous system disease. Given the considerable lack of effective treatments for age-related neurological disorders, new therapeutic approaches targeting the cell cycle machinery might thus be considered. This review aims at summarizing current knowledge about the role of the cell cycle machinery in post-mitotic neurons in healthy and pathological conditions.
    MeSH term(s) Animals ; Apoptosis/physiology ; Cell Cycle/physiology ; Cell Cycle Proteins/metabolism ; Humans ; Mitosis/physiology ; Nervous System Diseases/metabolism ; Nervous System Diseases/physiopathology ; Neurons/metabolism ; Neurons/physiology
    Chemical Substances Cell Cycle Proteins
    Language English
    Publishing date 2020-05-31
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 1358415-7
    ISSN 1420-9071 ; 1420-682X
    ISSN (online) 1420-9071
    ISSN 1420-682X
    DOI 10.1007/s00018-020-03548-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 195: Show issues Location:
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    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  5. Article: Mechanisms and Functional Significance of Stroke-Induced Neurogenesis.

    Marlier, Quentin / Verteneuil, Sebastien / Vandenbosch, Renaud / Malgrange, Brigitte

    Frontiers in neuroscience

    2015  Volume 9, Page(s) 458

    Abstract: Stroke affects one in every six people worldwide, and is the leading cause of adult disability. After stroke, some limited spontaneous recovery occurs, the mechanisms of which remain largely unknown. Multiple, parallel approaches are being investigated ... ...

    Abstract Stroke affects one in every six people worldwide, and is the leading cause of adult disability. After stroke, some limited spontaneous recovery occurs, the mechanisms of which remain largely unknown. Multiple, parallel approaches are being investigated to develop neuroprotective, reparative and regenerative strategies for the treatment of stroke. For years, clinical studies have tried to use exogenous cell therapy as a means of brain repair, with varying success. Since the rediscovery of adult neurogenesis and the identification of adult neural stem cells in the late nineties, one promising field of investigation is focused upon triggering and stimulating this self-repair system to replace the neurons lost following brain injury. For instance, it is has been demonstrated that the adult brain has the capacity to produce large numbers of new neurons in response to stroke. The purpose of this review is to provide an updated overview of stroke-induced adult neurogenesis, from a cellular and molecular perspective, to its impact on brain repair and functional recovery.
    Language English
    Publishing date 2015-12-08
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2411902-7
    ISSN 1662-453X ; 1662-4548
    ISSN (online) 1662-453X
    ISSN 1662-4548
    DOI 10.3389/fnins.2015.00458
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Genetic and pharmacological inhibition of Cdk1 provides neuroprotection towards ischemic neuronal death.

    Marlier, Quentin / Jibassia, Florian / Verteneuil, Sébastien / Linden, Jérôme / Kaldis, Philipp / Meijer, Laurent / Nguyen, Laurent / Vandenbosch, Renaud / Malgrange, Brigitte

    Cell death discovery

    2018  Volume 4, Page(s) 43

    Abstract: Cell cycle proteins are mainly expressed by dividing cells. However, it is well established that these molecules play additional non-canonical activities in several cell death contexts. Increasing evidence shows expression of cell cycle regulating ... ...

    Abstract Cell cycle proteins are mainly expressed by dividing cells. However, it is well established that these molecules play additional non-canonical activities in several cell death contexts. Increasing evidence shows expression of cell cycle regulating proteins in post-mitotic cells, including mature neurons, following neuronal insult. Several cyclin-dependent kinases (Cdks) have already been shown to mediate ischemic neuronal death but Cdk1, a major cell cycle G2/M regulator, has not been investigated in this context. We therefore examined the role of Cdk1 in neuronal cell death following cerebral ischemia, using both in vitro and in vivo genetic and pharmacological approaches. Exposure of primary cortical neurons cultures to 4 h of oxygen-glucose deprivation (OGD) resulted in neuronal cell death and induced Cdk1 expression. Neurons from Cdk1-cKO mice showed partial resistance to OGD-induced neuronal cell death. Addition of R-roscovitine to the culture medium conferred neuroprotection against OGD-induced neuronal death. Transient 1-h occlusion of the cerebral artery (MCAO) also leads to Cdk1 expression and activation. Cdk1-cKO mice displayed partial resistance to transient 1-h MCAO. Moreover, systemic delivery of R-roscovitine was neuroprotective following transient 1-h MCAO. This study demonstrates that promising neuroprotective therapies can be considered through inhibition of the cell cycle machinery and particularly through pharmacological inhibition of Cdk1.
    Language English
    Publishing date 2018-03-16
    Publishing country United States
    Document type Journal Article
    ISSN 2058-7716
    ISSN 2058-7716
    DOI 10.1038/s41420-018-0044-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Proliferation of hippocampal progenitors relies on p27-dependent regulation of Cdk6 kinase activity.

    Caron, Nicolas / Genin, Emmanuelle C / Marlier, Quentin / Verteneuil, Sébastien / Beukelaers, Pierre / Morel, Laurence / Hu, Miaofen G / Hinds, Philip W / Nguyen, Laurent / Vandenbosch, Renaud / Malgrange, Brigitte

    Cellular and molecular life sciences : CMLS

    2018  Volume 75, Issue 20, Page(s) 3817–3827

    Abstract: Neural stem cells give rise to granule dentate neurons throughout life in the hippocampus. Upon activation, these stem cells generate fast proliferating progenitors that complete several rounds of divisions before differentiating into neurons. Although ... ...

    Abstract Neural stem cells give rise to granule dentate neurons throughout life in the hippocampus. Upon activation, these stem cells generate fast proliferating progenitors that complete several rounds of divisions before differentiating into neurons. Although the mechanisms regulating the activation of stem cells have been intensively studied, little attention has been given so far to the intrinsic machinery allowing the expansion of the progenitor pool. The cell cycle protein Cdk6 positively regulates the proliferation of hippocampal progenitors, but the mechanism involved remains elusive. Whereas Cdk6 functions primarily as a cell cycle kinase, it can also act as transcriptional regulator in cancer cells and hematopoietic stem cells. Using mouse genetics, we show here that the function of Cdk6 in hippocampal neurogenesis relies specifically on its kinase activity. The present study also reveals a specific regulatory mechanism for Cdk6 in hippocampal progenitors. In contrast to the classical model of the cell cycle, we observe that the Cip/Kip family member p27, rather than the Ink4 family, negatively regulates Cdk6 in the adult hippocampus. Altogether, our data uncover a unique, cell type-specific regulatory mechanism controlling the expansion of hippocampal progenitors, where Cdk6 kinase activity is modulated by p27.
    MeSH term(s) Animals ; Cell Proliferation ; Cyclin-Dependent Kinase 2/metabolism ; Cyclin-Dependent Kinase 6/genetics ; Cyclin-Dependent Kinase 6/metabolism ; Cyclin-Dependent Kinase Inhibitor p18/deficiency ; Cyclin-Dependent Kinase Inhibitor p18/genetics ; Cyclin-Dependent Kinase Inhibitor p27/genetics ; Cyclin-Dependent Kinase Inhibitor p27/metabolism ; Dentate Gyrus/metabolism ; Dentate Gyrus/pathology ; Hippocampus/cytology ; Hippocampus/metabolism ; Hippocampus/pathology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mutagenesis, Site-Directed ; Neural Stem Cells/cytology ; Neural Stem Cells/metabolism ; Neurogenesis
    Chemical Substances Cyclin-Dependent Kinase Inhibitor p18 ; Cyclin-Dependent Kinase Inhibitor p27 (147604-94-2) ; Cyclin-Dependent Kinase 2 (EC 2.7.11.22) ; Cyclin-Dependent Kinase 6 (EC 2.7.11.22)
    Language English
    Publishing date 2018-05-04
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 1358415-7
    ISSN 1420-9071 ; 1420-682X
    ISSN (online) 1420-9071
    ISSN 1420-682X
    DOI 10.1007/s00018-018-2832-x
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 195: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  8. Article: Champignons sauvages comestibles d'un territoire de forêt claire zambézienne (Province de Copperbelt, Zambie)

    Bourdeaux, Quentin / Buyck, B. / Malaisse, François / Matera, J. / Marlier, Michel / Wathelet, Bernard / Lognay, Georges
    Language English
    Document type Article
    ISSN 0379-0452
    Database AGRIS - International Information System for the Agricultural Sciences and Technology

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