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  1. AU="Bagnard, Dominique"
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  1. Book: Axon growth and guidance

    Bagnard, Dominique

    (Advances in experimental medicine and biology ; 621)

    2007  

    Author's details ed. by Dominique Bagnard
    Series title Advances in experimental medicine and biology ; 621
    Collection
    Keywords Nerve Regeneration ; Axons / physiology ; Nervous System / growth and development
    Language English
    Size XVI, 169 S. : Ill., graph. Darst.
    Publisher Springer u.a.
    Publishing place New York
    Publishing country United States
    Document type Book
    HBZ-ID HT015462223
    ISBN 978-0-387-76714-7 ; 0-387-76714-2
    Database Catalogue ZB MED Medicine, Health

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  2. Book: Neuropilin

    Bagnard, Dominique

    from nervous system to vascular and tumor biology

    (Advances in experimental medicine and biology ; 515)

    2002  

    Author's details ed. by Dominique Bagnard
    Series title Advances in experimental medicine and biology ; 515
    Collection
    Keywords Nerve Tissue Proteins / chemistry ; Vascular Cell Adhesion Molecule-1 ; Receptor, Epidermal Growth Factor ; Neuropiline ; Neuropil
    Subject Neuropilem
    Language English
    Size XIII, 142 S. : Ill., graph. Darst.
    Publisher Kluwer/Plenum
    Publishing place New York u.a.
    Publishing country United States
    Document type Book
    HBZ-ID HT013573199
    ISBN 0-306-47416-6 ; 978-0-306-47416-3
    Database Catalogue ZB MED Medicine, Health

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  3. Article: Manipulating Macrophage/Microglia Polarization to Treat Glioblastoma or Multiple Sclerosis.

    Kuntzel, Thomas / Bagnard, Dominique

    Pharmaceutics

    2022  Volume 14, Issue 2

    Abstract: Macrophages and microglia are implicated in several diseases with divergent roles in physiopathology. This discrepancy can be explained by their capacity to endorse different polarization states. Theoretical extremes of these states are called M1 and M2. ...

    Abstract Macrophages and microglia are implicated in several diseases with divergent roles in physiopathology. This discrepancy can be explained by their capacity to endorse different polarization states. Theoretical extremes of these states are called M1 and M2. M1 are pro-inflammatory, microbicidal, and cytotoxic whereas M2 are anti-inflammatory, immunoregulatory cells in favor of tumor progression. In pathological states, these polarizations are dysregulated, thus restoring phenotypes could be an interesting treatment approach against diseases. In this review, we will focus on compounds targeting macrophages and microglia polarization in two very distinctive pathologies: multiple sclerosis and glioblastoma. Multiple sclerosis is an inflammatory disease characterized by demyelination and axon degradation. In this case, macrophages and microglia endorse a M1-like phenotype inducing inflammation. Promoting the opposite M2-like polarization could be an interesting treatment strategy. Glioblastoma is a brain tumor in which macrophages and microglia facilitate tumor progression, spreading, and angiogenesis. They are part of the tumor associated macrophages displaying an anti-inflammatory phenotype, thereby inhibiting anti-tumoral immunity. Re-activating them could be a method to limit and reduce tumor progression. These two pathologies will be used to exemplify that targeting the polarization of macrophages and microglia is a promising approach with a broad spectrum of applications deserving more attention.
    Language English
    Publishing date 2022-02-01
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2527217-2
    ISSN 1999-4923
    ISSN 1999-4923
    DOI 10.3390/pharmaceutics14020344
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Manipulating oligodendrocyte intrinsic regeneration mechanism to promote remyelination

    Binamé, Fabien / Pham-Van, Lucas D. / Bagnard, Dominique

    Cellular and molecular life sciences. 2021 July, v. 78, no. 13

    2021  

    Abstract: In demyelinated lesions, astrocytes, activated microglia and infiltrating macrophages secrete several factors regulating oligodendrocyte precursor cells’ behaviour. What appears to be the initiation of an intrinsic mechanism of myelin repair is only ... ...

    Abstract In demyelinated lesions, astrocytes, activated microglia and infiltrating macrophages secrete several factors regulating oligodendrocyte precursor cells’ behaviour. What appears to be the initiation of an intrinsic mechanism of myelin repair is only leading to partial recovery and inefficient remyelination, a process worsening over the course of the disease. This failure is largely due to the concomitant accumulation of inhibitory cues in and around the lesion sites opposing to growth promoting factors. Here starts a complex game of interactions between the signalling pathways controlling oligodendrocytes migration or differentiation. Receptors of positive or negative cues are modulating Ras, PI3K or RhoGTPases pathways acting on oligodendrocyte cytoskeleton remodelling. From the description of this intricate signalling network, this review addresses the extent to which the modulation of the global response to inhibitory cues may pave the route towards novel therapeutic approaches for myelin repair.
    Keywords astrocytes ; cytoskeleton ; macrophages ; myelin sheath ; oligodendroglia ; phosphatidylinositol 3-kinase ; therapeutics
    Language English
    Dates of publication 2021-07
    Size p. 5257-5273.
    Publishing place Springer International Publishing
    Document type Article
    Note Review
    ZDB-ID 1358415-7
    ISSN 1420-9071 ; 1420-682X
    ISSN (online) 1420-9071
    ISSN 1420-682X
    DOI 10.1007/s00018-021-03852-4
    Database NAL-Catalogue (AGRICOLA)

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  5. Article ; Online: The Translatability of Multiple Sclerosis Animal Models for Biomarkers Discovery and Their Clinical Use.

    Birmpili, Dafni / Charmarke Askar, Imane / Bigaut, Kévin / Bagnard, Dominique

    International journal of molecular sciences

    2022  Volume 23, Issue 19

    Abstract: Multiple Sclerosis (MS) is a chronic autoimmune disease affecting the central nervous system which is characterized by demyelinating lesions and axonal damage. MS is a complex disease characterized by important pathophysiological heterogeneity affecting ... ...

    Abstract Multiple Sclerosis (MS) is a chronic autoimmune disease affecting the central nervous system which is characterized by demyelinating lesions and axonal damage. MS is a complex disease characterized by important pathophysiological heterogeneity affecting the clinical appearance, progression and therapeutic response for each patient. Therefore, there is a strong unmet need to define specific biomarkers that will reflect the different features of the disease. Experimental autoimmune encephalomyelitis (EAE) is the most commonly used experimental model for the study of MS, as it resembles the pathological features of human MS in many aspects and has allowed for the elucidation of pathogenesis pathways and the validation of certain targets for MS therapies. In this review, we discuss clinically relevant MS molecular biomarkers, divided into five groups based on the key pathological hallmarks of MS: inflammation, blood-brain barrier disruption, myelin and axonal damage, gliosis and, ultimately, repair mechanisms. To address the feasibility of translation between the animal model and human disease, we present an overview of several molecular biomarkers of each category and compare their respective deregulation patterns. We conclude that, like any disease animal model, EAE models can sometimes fail to mimic the entire spectrum of human disease, but they can nonetheless recapitulate the disease's primary hallmarks. We show that the EAE model is a valuable tool for understanding MS physiopathological mechanisms and for identifying biomarkers fundamental for drug development.
    MeSH term(s) Animals ; Biomarkers ; Central Nervous System/pathology ; Disease Models, Animal ; Encephalomyelitis, Autoimmune, Experimental/pathology ; Humans ; Multiple Sclerosis/pathology ; Myelin Sheath/pathology
    Chemical Substances Biomarkers
    Language English
    Publishing date 2022-09-29
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms231911532
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Manipulating oligodendrocyte intrinsic regeneration mechanism to promote remyelination.

    Binamé, Fabien / Pham-Van, Lucas D / Bagnard, Dominique

    Cellular and molecular life sciences : CMLS

    2021  Volume 78, Issue 13, Page(s) 5257–5273

    Abstract: In demyelinated lesions, astrocytes, activated microglia and infiltrating macrophages secrete several factors regulating oligodendrocyte precursor cells' behaviour. What appears to be the initiation of an intrinsic mechanism of myelin repair is only ... ...

    Abstract In demyelinated lesions, astrocytes, activated microglia and infiltrating macrophages secrete several factors regulating oligodendrocyte precursor cells' behaviour. What appears to be the initiation of an intrinsic mechanism of myelin repair is only leading to partial recovery and inefficient remyelination, a process worsening over the course of the disease. This failure is largely due to the concomitant accumulation of inhibitory cues in and around the lesion sites opposing to growth promoting factors. Here starts a complex game of interactions between the signalling pathways controlling oligodendrocytes migration or differentiation. Receptors of positive or negative cues are modulating Ras, PI3K or RhoGTPases pathways acting on oligodendrocyte cytoskeleton remodelling. From the description of this intricate signalling network, this review addresses the extent to which the modulation of the global response to inhibitory cues may pave the route towards novel therapeutic approaches for myelin repair.
    MeSH term(s) Animals ; Cell Differentiation ; Humans ; Multiple Sclerosis/therapy ; Oligodendroglia/cytology ; Oligodendroglia/physiology ; Regeneration ; Remyelination
    Language English
    Publishing date 2021-05-21
    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/s00018-021-03852-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Increased stability of the TM helix oligomer abrogates the apoptotic activity of the human Fas receptor.

    Steindorf, Dominik / Loeuillet, Aurore / Bagnard, Dominique / Strand, Susanne / Schneider, Dirk

    Biochimica et biophysica acta. Biomembranes

    2021  Volume 1864, Issue 1, Page(s) 183807

    Abstract: Human death receptors control apoptotic events during cell differentiation, cell homeostasis and the elimination of damaged or infected cells. Receptor activation involves ligand-induced structural reorganizations of preformed receptor trimers. Here we ... ...

    Abstract Human death receptors control apoptotic events during cell differentiation, cell homeostasis and the elimination of damaged or infected cells. Receptor activation involves ligand-induced structural reorganizations of preformed receptor trimers. Here we show that the death receptor transmembrane domains only have a weak intrinsic tendency to homo-oligomerize within a membrane, and thus these domains potentially do not significantly contribute to receptor trimerization. However, mutation of Pro183 in the human CD95/Fas receptor transmembrane helix results in a dramatically increased interaction propensity, as shown by genetic assays. The increased interaction of the transmembrane domain is coupled with a decreased ligand-sensitivity of cells expressing the Fas receptor, and thus in a decreased number of apoptotic events. Mutation of Pro183 likely results in a substantial rearrangement of the self-associated Fas receptor transmembrane trimer, which likely abolishes further signaling of the apoptotic signal but may activate other signaling pathways. Our study shows that formation of a stable Fas receptor transmembrane helix oligomer does not per se result in receptor activation.
    MeSH term(s) Apoptosis/genetics ; Cell Differentiation/genetics ; Homeostasis/genetics ; Humans ; Ligands ; Mutation/genetics ; Protein Domains/genetics ; Protein Multimerization/genetics ; Receptors, Death Domain/genetics ; Signal Transduction/genetics ; fas Receptor/genetics
    Chemical Substances Ligands ; Receptors, Death Domain ; fas Receptor
    Language English
    Publishing date 2021-10-15
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 60-7
    ISSN 1879-2642 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    ISSN (online) 1879-2642 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2618 ; 1879-2650
    ISSN 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    DOI 10.1016/j.bbamem.2021.183807
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Implication of the Transmembrane Domain in the Interleukin 10 Receptor Platform Oligomerisation.

    Kuntzel, Thomas / Spenlé, Caroline / Pham-Van, Lucas D / Birmpili, Dafni / Riou, Aurélien / Loeuillet, Aurore / Charmarke-Askar, Imane / Bagnard, Dominique

    Cells

    2023  Volume 12, Issue 10

    Abstract: Interleukin 10 (IL-10) exerts anti-inflammatory and immune regulatory roles through its fixation to the IL-10 receptor (IL-10R). The two subunits (IL-10Rα and IL-10Rβ) organise themselves to form a hetero-tetramer to induce the activation of the ... ...

    Abstract Interleukin 10 (IL-10) exerts anti-inflammatory and immune regulatory roles through its fixation to the IL-10 receptor (IL-10R). The two subunits (IL-10Rα and IL-10Rβ) organise themselves to form a hetero-tetramer to induce the activation of the transcription factor STAT3. We analysed the activation patterns of the IL-10R, especially the contribution of the transmembrane (TM) domain of the IL-10Rα and IL-10Rβ subunits, as evidence accumulates that this short domain has tremendous implications in receptor oligomerisation and activation. We also addressed whether targeting the TM domain of IL-10R with peptides mimicking the TM sequences of the subunits translates into biological consequences. The results illustrate the involvement of the TM domains from both subunits in receptor activation and feature a distinctive amino acid crucial for the interaction. The TM peptide targeting approach also appears to be suitable for modulating the activation of the receptor through its action on the dimerization capabilities of the TM domains and thereby constitutes a potential new strategy for the modulation of the inflammation in pathologic contexts.
    MeSH term(s) Receptors, Interleukin-10 ; Transcription Factors ; Gene Expression Regulation ; Signal Transduction ; Amino Acids
    Chemical Substances Receptors, Interleukin-10 ; Transcription Factors ; Amino Acids
    Language English
    Publishing date 2023-05-10
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells12101361
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Prediction of Drug Efficacy in Colon Cancer Preclinical Models Using a Novel Ranking Method of Gene Expression.

    Fritz, Justine / Lefebvre, Olivier / Fernandez, Aurore / Schmidt, Jordane / Bagnard, Dominique

    Cancers

    2020  Volume 12, Issue 1

    Abstract: The presence of stromal cells in tumors is altering the significance of molecular profiling when using standard methods of gene expression quantification. We developed a novel normalization method to rank target gene expression in tumor samples by ... ...

    Abstract The presence of stromal cells in tumors is altering the significance of molecular profiling when using standard methods of gene expression quantification. We developed a novel normalization method to rank target gene expression in tumor samples by comparisons with reference samples representing the different cell types found in a tumor. The score for each target gene obtained after normalization, is aimed to be predictive of targeted therapies efficiency. We performed this qPCR analysis on human colorectal cancers to demonstrate the importance of reference samples to obtain accurate data and on a collection of patient-derived xenografted (PDX) colon tumors treated with Cetuximab (anti-EGFR) to demonstrate that the calculated EGFR score is predictive of Cetuximab efficacy. Interestingly, the score allowed to select an efficient treatment in a PDX model refractory to standard of care. This method is opening a novel way to predict targeted therapy efficiency which could be extended to several tumor types, and to unlimited target genes.
    Language English
    Publishing date 2020-01-08
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers12010149
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Book: Axon growth and guidance

    Bagnard, Dominique

    (Advances in experimental medicine and biology ; v. 621)

    2007  

    Author's details edited by Dominique Bagnard
    Series title Advances in experimental medicine and biology ; v. 621
    MeSH term(s) Axons/physiology ; Nerve Regeneration ; Nervous System/growth & development
    Language English
    Size xvi, 169 p. :, ill., port.
    Publisher Springer Science + Business Media ; Landes Bioscience
    Publishing place New York ; Austin, Tex
    Document type Book
    ISBN 9780387767147 ; 0387767142
    Database Catalogue of the US National Library of Medicine (NLM)

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