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  1. Article: Activated microglia release β-galactosidase that promotes inflammatory neurodegeneration.

    Kitchener, Emily J A / Dundee, Jacob M / Brown, Guy C

    Frontiers in aging neuroscience

    2024  Volume 15, Page(s) 1327756

    Abstract: Beta (β)-galactosidase is a lysosomal enzyme that removes terminal galactose residues from glycolipids and glycoproteins. It is upregulated in, and used as a marker for, senescent cells. Microglia are brain macrophages implicated in neurodegeneration, ... ...

    Abstract Beta (β)-galactosidase is a lysosomal enzyme that removes terminal galactose residues from glycolipids and glycoproteins. It is upregulated in, and used as a marker for, senescent cells. Microglia are brain macrophages implicated in neurodegeneration, and can upregulate β-galactosidase when senescent. We find that inflammatory activation of microglia induced by lipopolysaccharide results in translocation of β-galactosidase to the cell surface and release into the medium. Similarly, microglia in aged mouse brains appear to have more β-galactosidase on their surface. Addition of β-galactosidase to neuronal-glial cultures causes microglial activation and neuronal loss mediated by microglia. Inhibition of β-galactosidase in neuronal-glial cultures reduces inflammation and neuronal loss induced by lipopolysaccharide. Thus, activated microglia release β-galactosidase that promotes microglial-mediated neurodegeneration which is prevented by inhibition of β-galactosidase.
    Language English
    Publishing date 2024-01-12
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2558898-9
    ISSN 1663-4365
    ISSN 1663-4365
    DOI 10.3389/fnagi.2023.1327756
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: P2Y

    Dundee, Jacob M / Puigdellívol, Mar / Butler, Richard / Brown, Guy C

    The Journal of neuroscience : the official journal of the Society for Neuroscience

    2023  Volume 43, Issue 48, Page(s) 8090–8103

    Abstract: During brain development, excess synapses are pruned (i.e., removed), in part by microglial phagocytosis, and dysregulated synaptic pruning can lead to behavioral deficits. The ... ...

    Abstract During brain development, excess synapses are pruned (i.e., removed), in part by microglial phagocytosis, and dysregulated synaptic pruning can lead to behavioral deficits. The P2Y
    MeSH term(s) Male ; Female ; Mice ; Animals ; Microglia/physiology ; Synapses ; Phagocytosis/physiology ; Neurons
    Chemical Substances purinoceptor P2Y6
    Language English
    Publishing date 2023-11-29
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 604637-x
    ISSN 1529-2401 ; 0270-6474
    ISSN (online) 1529-2401
    ISSN 0270-6474
    DOI 10.1523/JNEUROSCI.1089-23.2023
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1668: 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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  3. Article ; Online: P2Y

    Dundee, Jacob M / Puigdellívol, Mar / Butler, Richard / Cockram, Thomas O J / Brown, Guy C

    Aging cell

    2022  Volume 22, Issue 2, Page(s) e13761

    Abstract: Aging causes loss of brain synapses and memory, and microglial phagocytosis of synapses may contribute to this loss. Stressed neurons can release the nucleotide UTP, which is rapidly converted into UDP, that in turn activates the ... ...

    Abstract Aging causes loss of brain synapses and memory, and microglial phagocytosis of synapses may contribute to this loss. Stressed neurons can release the nucleotide UTP, which is rapidly converted into UDP, that in turn activates the P2Y
    MeSH term(s) Animals ; Mice ; Memory Disorders ; Mice, Knockout ; Microglia ; Phagocytosis/physiology ; Synapses
    Chemical Substances purinoceptor P2Y6
    Language English
    Publishing date 2022-12-24
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2113083-8
    ISSN 1474-9726 ; 1474-9718
    ISSN (online) 1474-9726
    ISSN 1474-9718
    DOI 10.1111/acel.13761
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6581: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  4. Article: Latent Epigenetic Programs in Müller Glia Contribute to Stress, Injury, and Disease Response in the Retina.

    Norrie, Jackie L / Lupo, Marybeth / Shirinifard, Abbas / Djekidel, Nadhir / Ramirez, Cody / Xu, Beisi / Dundee, Jacob M / Dyer, Michael A

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Previous studies have demonstrated the dynamic changes in chromatin structure during retinal development that correlate with changes in gene expression. However, a major limitation of those prior studies was the lack of cellular resolution. Here, we ... ...

    Abstract Previous studies have demonstrated the dynamic changes in chromatin structure during retinal development that correlate with changes in gene expression. However, a major limitation of those prior studies was the lack of cellular resolution. Here, we integrate single-cell (sc) RNA-seq and scATAC-seq with bulk retinal data sets to identify cell type-specific changes in the chromatin structure during development. Although most genes' promoter activity is strongly correlated with chromatin accessibility, we discovered several hundred genes that were transcriptionally silent but had accessible chromatin at their promoters. Most of those silent/accessible gene promoters were in the Müller glial cells. The Müller cells are radial glia of the retina and perform a variety of essential functions to maintain retinal homeostasis and respond to stress, injury, or disease. The silent/accessible genes in Müller glia are enriched in pathways related to inflammation, angiogenesis, and other types of cell-cell signaling and were rapidly activated when we tested 15 different physiologically relevant conditions to mimic retinal stress, injury, or disease in human and murine retinae. We refer to these as "pliancy genes" because they allow the Müller glia to rapidly change their gene expression and cellular state in response to different types of retinal insults. The Müller glial cell pliancy program is established during development, and we demonstrate that pliancy genes are necessary and sufficient for regulating inflammation in the murine retina in vivo. In zebrafish, Müller glia can de-differentiate and form retinal progenitor cells that replace lost neurons. The pro-inflammatory pliancy gene cascade is not activated in zebrafish Müller glia following injury, and we propose a model in which species-specific pliancy programs underly the differential response to retinal damage in species that can regenerate retinal neurons (zebrafish) versus those that cannot (humans and mice).
    Language English
    Publishing date 2023-10-17
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.10.15.562396
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: The Phagocytic Code Regulating Phagocytosis of Mammalian Cells.

    Cockram, Tom O J / Dundee, Jacob M / Popescu, Alma S / Brown, Guy C

    Frontiers in immunology

    2021  Volume 12, Page(s) 629979

    Abstract: Mammalian phagocytes can phagocytose (i.e. eat) other mammalian cells in the body if they display certain signals, and this phagocytosis plays fundamental roles in development, cell turnover, tissue homeostasis and disease prevention. To phagocytose the ... ...

    Abstract Mammalian phagocytes can phagocytose (i.e. eat) other mammalian cells in the body if they display certain signals, and this phagocytosis plays fundamental roles in development, cell turnover, tissue homeostasis and disease prevention. To phagocytose the correct cells, phagocytes must discriminate which cells to eat using a 'phagocytic code' - a set of over 50 known phagocytic signals determining whether a cell is eaten or not - comprising find-me signals, eat-me signals, don't-eat-me signals and opsonins. Most opsonins require binding to eat-me signals - for example, the opsonins galectin-3, calreticulin and C1q bind asialoglycan eat-me signals on target cells - to induce phagocytosis. Some proteins act as 'self-opsonins', while others are 'negative opsonins' or 'phagocyte suppressants', inhibiting phagocytosis. We review known phagocytic signals here, both established and novel, and how they integrate to regulate phagocytosis of several mammalian targets - including excess cells in development, senescent and aged cells, infected cells, cancer cells, dead or dying cells, cell debris and neuronal synapses. Understanding the phagocytic code, and how it goes wrong, may enable novel therapies for multiple pathologies with too much or too little phagocytosis, such as: infectious disease, cancer, neurodegeneration, psychiatric disease, cardiovascular disease, ageing and auto-immune disease.
    MeSH term(s) Animals ; Calreticulin/physiology ; Cellular Senescence ; Humans ; Intercellular Adhesion Molecule-3/physiology ; Opsonin Proteins/physiology ; Phagocytosis/physiology ; Phosphatidylserines/physiology ; Polysaccharides/physiology ; Signal Transduction/physiology ; Synapses/physiology
    Chemical Substances Calreticulin ; Intercellular Adhesion Molecule-3 ; Opsonin Proteins ; Phosphatidylserines ; Polysaccharides
    Language English
    Publishing date 2021-06-09
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2021.629979
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Inflammatory neuronal loss in the substantia nigra induced by systemic lipopolysaccharide is prevented by knockout of the P2Y

    Milde, Stefan / van Tartwijk, Francesca W / Vilalta, Anna / Hornik, Tamara C / Dundee, Jacob M / Puigdellívol, Mar / Brown, Guy C

    Journal of neuroinflammation

    2021  Volume 18, Issue 1, Page(s) 225

    Abstract: Inflammation may contribute to multiple brain pathologies. One cause of inflammation is lipopolysaccharide/endotoxin (LPS), the levels of which are elevated in blood and/or brain during bacterial infections, gut dysfunction and neurodegenerative diseases, ...

    Abstract Inflammation may contribute to multiple brain pathologies. One cause of inflammation is lipopolysaccharide/endotoxin (LPS), the levels of which are elevated in blood and/or brain during bacterial infections, gut dysfunction and neurodegenerative diseases, such as Parkinson's disease. How inflammation causes neuronal loss is unclear, but one potential mechanism is microglial phagocytosis of neurons, which is dependent on the microglial P2Y
    MeSH term(s) Animals ; Cell Line, Transformed ; Cells, Cultured ; Dopaminergic Neurons/drug effects ; Dopaminergic Neurons/metabolism ; Dopaminergic Neurons/pathology ; Inflammation/chemically induced ; Inflammation/metabolism ; Inflammation/pathology ; Lipopolysaccharides/toxicity ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neurons/drug effects ; Neurons/metabolism ; Neurons/pathology ; Organ Culture Techniques ; PC12 Cells ; Rats ; Receptors, Purinergic P2/deficiency ; Substantia Nigra/drug effects ; Substantia Nigra/metabolism ; Substantia Nigra/pathology
    Chemical Substances Lipopolysaccharides ; Receptors, Purinergic P2 ; purinoceptor P2Y6
    Language English
    Publishing date 2021-10-11
    Publishing country England
    Document type Journal Article
    ZDB-ID 2156455-3
    ISSN 1742-2094 ; 1742-2094
    ISSN (online) 1742-2094
    ISSN 1742-2094
    DOI 10.1186/s12974-021-02280-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: The microglial P2Y

    Puigdellívol, Mar / Milde, Stefan / Vilalta, Anna / Cockram, Tom O J / Allendorf, David H / Lee, Jeffrey Y / Dundee, Jacob M / Pampuščenko, Katryna / Borutaite, Vilmante / Nuthall, Hugh N / Brelstaff, Jack H / Spillantini, Maria Grazia / Brown, Guy C

    Cell reports

    2021  Volume 37, Issue 13, Page(s) 110148

    Abstract: Microglia are implicated in neurodegeneration, potentially by phagocytosing neurons, but it is unclear how to block the detrimental effects of microglia while preserving their beneficial roles. The microglial ... ...

    Abstract Microglia are implicated in neurodegeneration, potentially by phagocytosing neurons, but it is unclear how to block the detrimental effects of microglia while preserving their beneficial roles. The microglial P2Y
    Language English
    Publishing date 2021-12-26
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2021.110148
    Database MEDical Literature Analysis and Retrieval System OnLINE

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