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  1. Article ; Online: Microglial sex differences in innate high anxiety and modulatory effects of minocycline.

    Ugursu, Bilge / Sah, Anupam / Sartori, Simone / Popp, Oliver / Mertins, Philip / Dunay, Ildiko R / Kettenmann, Helmut / Singewald, Nicolas / Wolf, Susanne A

    Brain, behavior, and immunity

    2024  Volume 119, Page(s) 465–481

    Abstract: Microglia modulate synaptic refinement in the central nervous system (CNS). We have previously shown that a mouse model with innate high anxiety-related behavior (HAB) displays higher ... ...

    Abstract Microglia modulate synaptic refinement in the central nervous system (CNS). We have previously shown that a mouse model with innate high anxiety-related behavior (HAB) displays higher CD68
    Language English
    Publishing date 2024-03-27
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 639219-2
    ISSN 1090-2139 ; 0889-1591
    ISSN (online) 1090-2139
    ISSN 0889-1591
    DOI 10.1016/j.bbi.2024.03.035
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: An in vitro platform supports generation of human innate lymphoid cells from CD34

    Hernández, Daniela Carolina / Juelke, Kerstin / Müller, Nils Christian / Durek, Pawel / Ugursu, Bilge / Mashreghi, Mir-Farzin / Rückert, Timo / Romagnani, Chiara

    Immunity

    2021  Volume 54, Issue 10, Page(s) 2417–2432.e5

    Abstract: Innate lymphoid cells (ILCs) are critical effectors of innate immunity and inflammation, whose development and activation pathways make for attractive therapeutic targets. However, human ILC generation has not been systematically explored, and previous ... ...

    Abstract Innate lymphoid cells (ILCs) are critical effectors of innate immunity and inflammation, whose development and activation pathways make for attractive therapeutic targets. However, human ILC generation has not been systematically explored, and previous in vitro investigations relied on the analysis of few markers or cytokines, which are suboptimal to assign lineage identity. Here, we developed a platform that reliably generated human ILC lineages from CD34
    MeSH term(s) Antigens, CD34/immunology ; Cell Culture Techniques/methods ; Cell Differentiation/immunology ; Cell Lineage/immunology ; Hematopoietic Stem Cells/cytology ; Hematopoietic Stem Cells/immunology ; Humans ; Immunity, Innate/immunology ; Lymphocytes/cytology ; Lymphocytes/immunology ; Single-Cell Analysis/methods
    Chemical Substances Antigens, CD34
    Language English
    Publishing date 2021-08-27
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/j.immuni.2021.07.019
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Sex-specific microglia state in the Neuroligin-4 knock-out mouse model of autism spectrum disorder.

    Guneykaya, Dilansu / Ugursu, Bilge / Logiacco, Francesca / Popp, Oliver / Feiks, Maria Almut / Meyer, Niklas / Wendt, Stefan / Semtner, Marcus / Cherif, Fatma / Gauthier, Christian / Madore, Charlotte / Yin, Zhuoran / Çınar, Özcan / Arslan, Taner / Gerevich, Zoltan / Mertins, Philipp / Butovsky, Oleg / Kettenmann, Helmut / Wolf, Susanne A

    Brain, behavior, and immunity

    2023  Volume 111, Page(s) 61–75

    Abstract: Neuroligin-4 (NLGN4) loss-of-function mutations are associated with monogenic heritable autism spectrum disorder (ASD) and cause alterations in both synaptic and behavioral phenotypes. Microglia, the resident CNS macrophages, are implicated in ASD ... ...

    Abstract Neuroligin-4 (NLGN4) loss-of-function mutations are associated with monogenic heritable autism spectrum disorder (ASD) and cause alterations in both synaptic and behavioral phenotypes. Microglia, the resident CNS macrophages, are implicated in ASD development and progression. Here we studied the impact of NLGN4 loss in a mouse model, focusing on microglia phenotype and function in both male and female mice. NLGN4 depletion caused lower microglia density, less ramified morphology, reduced response to injury and purinergic signaling specifically in the hippocampal CA3 region predominantly in male mice. Proteomic analysis revealed disrupted energy metabolism in male microglia and provided further evidence for sexual dimorphism in the ASD associated microglial phenotype. In addition, we observed impaired gamma oscillations in a sex-dependent manner. Lastly, estradiol application in male NLGN4
    MeSH term(s) Male ; Female ; Animals ; Mice ; Autism Spectrum Disorder/genetics ; Microglia ; Mice, Knockout ; Proteomics ; Neurons/physiology
    Language English
    Publishing date 2023-03-29
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 639219-2
    ISSN 1090-2139 ; 0889-1591
    ISSN (online) 1090-2139
    ISSN 0889-1591
    DOI 10.1016/j.bbi.2023.03.023
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Microglia sense neuronal activity via GABA in the early postnatal hippocampus.

    Logiacco, Francesca / Xia, Pengfei / Georgiev, Svilen Veselinov / Franconi, Celeste / Chang, Yi-Jen / Ugursu, Bilge / Sporbert, Anje / Kühn, Ralf / Kettenmann, Helmut / Semtner, Marcus

    Cell reports

    2021  Volume 37, Issue 13, Page(s) 110128

    Abstract: Microglia, the resident macrophages in the central nervous system, express receptors for classical neurotransmitters, such as γ-aminobutyric acid (GABA) and glutamate, suggesting that they sense synaptic activity. To detect microglial ... ...

    Abstract Microglia, the resident macrophages in the central nervous system, express receptors for classical neurotransmitters, such as γ-aminobutyric acid (GABA) and glutamate, suggesting that they sense synaptic activity. To detect microglial Ca
    Language English
    Publishing date 2021-12-26
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2021.110128
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Deletion of muscarinic acetylcholine receptor 3 in microglia impacts brain ischemic injury.

    Costa, Amanda / Haage, Verena / Yang, Seulkee / Wegner, Stephanie / Ersoy, Burcu / Ugursu, Bilge / Rex, Andre / Kronenberg, Golo / Gertz, Karen / Endres, Matthias / Wolf, Susanne A / Kettenmann, Helmut

    Brain, behavior, and immunity

    2020  Volume 91, Page(s) 89–104

    Abstract: Microglia are the immune cells of the brain and become activated during any type of brain injury. In the middle cerebral artery occlusion (MCAo) model, a mouse model for ischemic stroke, we have previously shown that microglia and invaded monocytes ... ...

    Abstract Microglia are the immune cells of the brain and become activated during any type of brain injury. In the middle cerebral artery occlusion (MCAo) model, a mouse model for ischemic stroke, we have previously shown that microglia and invaded monocytes upregulate the expression of the muscarinic acetylcholine receptor 3 (M3R) in the ischemic lesion. Here we tested whether this upregulation has an impact on the pathogenesis of MCAo. We depleted the m3R receptor in microglia, but not in circulating monocytes by giving tamoxifen to CX3CR1-CreERT
    MeSH term(s) Animals ; Brain ; Brain Ischemia ; Disease Models, Animal ; Female ; Infarction, Middle Cerebral Artery ; Male ; Mice ; Mice, Inbred C57BL ; Microglia ; Receptor, Muscarinic M3/genetics ; Stroke
    Chemical Substances Receptor, Muscarinic M3
    Language English
    Publishing date 2020-09-12
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639219-2
    ISSN 1090-2139 ; 0889-1591
    ISSN (online) 1090-2139
    ISSN 0889-1591
    DOI 10.1016/j.bbi.2020.09.008
    Database MEDical Literature Analysis and Retrieval System OnLINE

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