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  1. Article ; Online: An attenuated immune response by Schwann cells and macrophages inhibits nerve regeneration in aged rats.

    Scheib, Jami L / Höke, Ahmet

    Neurobiology of aging

    2016  Volume 45, Page(s) 1–9

    Abstract: Although peripheral nerves are capable of regeneration, advanced age decreases the potential for functional recovery after injury. The cellular mechanisms for this are not currently understood. Here, we performed sciatic nerve grafting with young (2 ... ...

    Abstract Although peripheral nerves are capable of regeneration, advanced age decreases the potential for functional recovery after injury. The cellular mechanisms for this are not currently understood. Here, we performed sciatic nerve grafting with young (2 months old) and aged (18 months old) Brown-Norway male rats, in which 1 cm nerve grafts from young or aged rats were sutured into nerves of young or aged rats. Axons were allowed to regenerate until the nerve grafts and distal nerves were harvested at 1, 3, and 7 days and 2 and 6 weeks. At 6 weeks, our data suggested that young nerve grafts supported regeneration better than aged nerve grafts. In addition, myelin debris clearance was inhibited in young nerves when grafted into aged rats, but clearance was faster when aged nerves were grafted into young rats. Further analysis revealed that aged macrophages have delayed migration into injured nerve, and macrophages and Schwann cells from aged rats were less phagocytic for myelin debris in vitro. To understand these impairments, expression levels of pro- and anti-inflammatory cytokines were analyzed at 1 day after injury. Based on these levels, there was not a clear polarization to either an M1 or M2 phenotype; however, expression levels of IL-6, IL-10, CCL2 (MCP1), and Arg-1 were decreased in aged nerves. Taken together, both macrophages and Schwann cells had attenuated responses to nerve injury in aged rats, leading to inefficient clearance of debris and impaired axonal regeneration.
    MeSH term(s) Aging/immunology ; Aging/physiology ; Animals ; Cells, Cultured ; Chemokine CCL2/metabolism ; Interleukin-10/metabolism ; Interleukin-6/metabolism ; Macrophages/immunology ; Male ; Nerve Regeneration/immunology ; Rats ; Schwann Cells/immunology ; Sciatic Nerve/metabolism ; Sciatic Nerve/physiology
    Chemical Substances Ccl2 protein, rat ; Chemokine CCL2 ; Interleukin-6 ; Interleukin-10 (130068-27-8)
    Language English
    Publishing date 2016-09
    Publishing country United States
    Document type Journal Article
    ZDB-ID 604505-4
    ISSN 1558-1497 ; 0197-4580
    ISSN (online) 1558-1497
    ISSN 0197-4580
    DOI 10.1016/j.neurobiolaging.2016.05.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Eaters of the dead: glial precursors clear neuron corpses during development.

    Scheib, Jami L / Carter, Bruce D

    Cell cycle (Georgetown, Tex.)

    2010  Volume 9, Issue 10, Page(s) 1867–1868

    MeSH term(s) Animals ; Drosophila ; Drosophila Proteins/metabolism ; Membrane Proteins/metabolism ; Models, Biological ; Neuroglia/cytology ; Neuroglia/metabolism ; Neurons/cytology ; Neurons/metabolism ; Phagocytosis/physiology ; Schwann Cells/cytology ; Schwann Cells/metabolism
    Chemical Substances Drosophila Proteins ; Membrane Proteins
    Language English
    Publishing date 2010-05-15
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.4161/cc.9.10.11678
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Jedi-1 and MEGF10 signal engulfment of apoptotic neurons through the tyrosine kinase Syk.

    Scheib, Jami L / Sullivan, Chelsea S / Carter, Bruce D

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

    2012  Volume 32, Issue 38, Page(s) 13022–13031

    Abstract: During the development of the peripheral nervous system there is extensive apoptosis, and these neuronal corpses need to be cleared to prevent an inflammatory response. Recently, Jedi-1 and MEGF10, both expressed in glial precursor cells, were identified ...

    Abstract During the development of the peripheral nervous system there is extensive apoptosis, and these neuronal corpses need to be cleared to prevent an inflammatory response. Recently, Jedi-1 and MEGF10, both expressed in glial precursor cells, were identified in mouse as having an essential role in this phagocytosis (Wu et al., 2009); however, the mechanisms by which they promote engulfment remained unknown. Both Jedi-1 and MEGF10 are homologous to the Drosophila melanogaster receptor Draper, which mediates engulfment through activation of the tyrosine kinase Shark. Here, we identify Syk, the mammalian homolog of Shark, as a signal transducer for both Jedi-1 and MEGF10. Syk interacted with each receptor independently through the immunoreceptor tyrosine-based activation motifs (ITAMs) in their intracellular domains. The interaction was enhanced by phosphorylation of the tyrosines in the ITAMs by Src family kinases (SFKs). Jedi association with Syk and activation of the kinase was also induced by exposure to dead cells. Expression of either Jedi-1 or MEGF10 in HeLa cells facilitated engulfment of carboxylated microspheres to a similar extent, and there was no additive effect when they were coexpressed. Mutation of the ITAM tyrosines of Jedi-1 and MEGF10 prevented engulfment. The SFK inhibitor PP2 or a selective Syk inhibitor (BAY 61-3606) also blocked engulfment. Similarly, in cocultures of glial precursors and dying sensory neurons from embryonic mice, addition of PP2 or knock down of endogenous Syk decreased the phagocytosis of apoptotic neurons. These results indicate that both Jedi-1 and MEGF10 can mediate phagocytosis independently through the recruitment of Syk.
    MeSH term(s) Amino Acid Motifs ; Animals ; Apoptosis/genetics ; Arabidopsis Proteins/metabolism ; Cell Count ; Cells, Cultured ; Coculture Techniques ; Embryo, Mammalian ; Enzyme Inhibitors/pharmacology ; Female ; Ganglia, Spinal/cytology ; Gene Expression Regulation/drug effects ; Gene Expression Regulation/genetics ; Green Fluorescent Proteins/genetics ; Humans ; Immunoprecipitation ; Immunoreceptor Tyrosine-Based Activation Motif/drug effects ; Immunoreceptor Tyrosine-Based Activation Motif/genetics ; Immunoreceptor Tyrosine-Based Activation Motif/physiology ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Intramolecular Transferases/metabolism ; Male ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Microglia ; Mutagenesis, Site-Directed ; Mutation/genetics ; Neurons ; Niacinamide/analogs & derivatives ; Niacinamide/pharmacology ; Phagocytosis/drug effects ; Phagocytosis/genetics ; Phosphorylation/drug effects ; Phosphorylation/genetics ; Protein-Tyrosine Kinases/genetics ; Protein-Tyrosine Kinases/metabolism ; Pyrimidines/pharmacology ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; Signal Transduction/drug effects ; Signal Transduction/genetics ; Staurosporine/pharmacology ; Syk Kinase ; Transfection
    Chemical Substances 2-(7-(3,4-dimethoxyphenyl)imidazo(1,2-c)pyrimidin-5-ylamino)nicotinamide ; Arabidopsis Proteins ; Enzyme Inhibitors ; Intracellular Signaling Peptides and Proteins ; Jedi protein, mouse ; Megf10 protein, mouse ; Membrane Proteins ; Pyrimidines ; RNA, Small Interfering ; Green Fluorescent Proteins (147336-22-9) ; Niacinamide (25X51I8RD4) ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; SYK protein, human (EC 2.7.10.2) ; Syk Kinase (EC 2.7.10.2) ; Syk protein, mouse (EC 2.7.10.2) ; Intramolecular Transferases (EC 5.4.-) ; marneral synthase, Arabidopsis (EC 5.4.-) ; Staurosporine (H88EPA0A3N)
    Language English
    Publishing date 2012-09-19
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 604637-x
    ISSN 1529-2401 ; 0270-6474
    ISSN (online) 1529-2401
    ISSN 0270-6474
    DOI 10.1523/JNEUROSCI.6350-11.2012
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Motor memory preservation in aged monkeys mirrors that of aged humans on a similar task.

    Walton, Ashley / Scheib, Jami L / McLean, Sheila / Zhang, Zhiming / Grondin, Richard

    Neurobiology of aging

    2008  Volume 29, Issue 10, Page(s) 1556–1562

    Abstract: We studied long-term motor memory preservation in rhesus monkeys tested on a task similar to that employed in humans. First, motor speed and rate of motor decline was measured in 23 animals ranging from 4 to 26 years old. The task for the animals ... ...

    Abstract We studied long-term motor memory preservation in rhesus monkeys tested on a task similar to that employed in humans. First, motor speed and rate of motor decline was measured in 23 animals ranging from 4 to 26 years old. The task for the animals consisted of removing a food reward from a curved rod within the inner chamber of an automated panel. Young animals performed twice as fast as the aged animals. Second, young (n=6) and aged (n=10) animals were re-tested 1 year later on the same task with no intervening practice. We anticipated a decline in motor speed of 144 ms/year, instead the average performance time recorded during the repeat session improved significantly by 17% in the aged animals. This finding mirrors that of a longitudinal study conducted in humans using a similar test panel and supports that, while initial performance times of a novel motor task decline with age, motor memory traces are preserved over an extended time interval, even without continued practice. The data also support that the rhesus monkey could be used as a model to study the mechanisms by which long-term retention of motor memory occurs in aging.
    MeSH term(s) Aging/physiology ; Aging/psychology ; Animals ; Brain/physiology ; Cognition/physiology ; Cross-Sectional Studies ; Disease Models, Animal ; Female ; Longitudinal Studies ; Macaca mulatta/physiology ; Macaca mulatta/psychology ; Memory/physiology ; Mental Processes/physiology ; Models, Neurological ; Neuropsychological Tests ; Psychomotor Performance/physiology ; Reaction Time/physiology ; Species Specificity ; Time Factors
    Language English
    Publishing date 2008-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 604505-4
    ISSN 1558-1497 ; 0197-4580
    ISSN (online) 1558-1497
    ISSN 0197-4580
    DOI 10.1016/j.neurobiolaging.2007.03.016
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: The adaptor protein GULP promotes Jedi-1-mediated phagocytosis through a clathrin-dependent mechanism.

    Sullivan, Chelsea S / Scheib, Jami L / Ma, Zhong / Dang, Rajan P / Schafer, Johanna M / Hickman, Francis E / Brodsky, Frances M / Ravichandran, Kodi S / Carter, Bruce D

    Molecular biology of the cell

    2014  Volume 25, Issue 12, Page(s) 1925–1936

    Abstract: During the development of the peripheral nervous system, the large number of apoptotic neurons generated are phagocytosed by glial precursor cells. This clearance is mediated, in part, through the mammalian engulfment receptor Jedi-1. However, the ... ...

    Abstract During the development of the peripheral nervous system, the large number of apoptotic neurons generated are phagocytosed by glial precursor cells. This clearance is mediated, in part, through the mammalian engulfment receptor Jedi-1. However, the mechanisms by which Jedi-1 mediates phagocytosis are poorly understood. Here we demonstrate that Jedi-1 associates with GULP, the mammalian homologue of CED-6, an adaptor protein required for phagocytosis mediated by the nematode engulfment receptor CED-1. Silencing GULP or mutating the NPXY motif in Jedi-1, which is required for GULP binding, prevents Jedi-1-mediated phagocytosis. How GULP promotes engulfment is not known. Of interest, we find that Jedi-1-induced phagocytosis requires GULP binding to clathrin heavy chain (CHC). During engulfment, CHC is tyrosine phosphorylated, which is required for Jedi-mediated engulfment. Both phosphoclathrin and actin accumulate around engulfed microspheres. Furthermore, knockdown of CHC in HeLa cells prevents Jedi-1-mediated engulfment of microspheres, and knockdown in glial precursors prevents the engulfment of apoptotic neurons. Taken together, these results reveal that Jedi-1 signals through recruitment of GULP, which promotes phagocytosis through a noncanonical phosphoclathrin-dependent mechanism.
    MeSH term(s) 3T3 Cells ; Actins/metabolism ; Adaptor Proteins, Signal Transducing/physiology ; Amino Acid Motifs ; Animals ; Clathrin/metabolism ; HeLa Cells ; Humans ; Membrane Proteins/chemistry ; Membrane Proteins/metabolism ; Mice ; Phagocytosis ; Protein Interaction Domains and Motifs ; Protein Transport
    Chemical Substances Actins ; Adaptor Proteins, Signal Transducing ; Clathrin ; GULP protein, mouse ; Jedi protein, mouse ; Membrane Proteins
    Language English
    Publishing date 2014-04-17
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1098979-1
    ISSN 1939-4586 ; 1059-1524
    ISSN (online) 1939-4586
    ISSN 1059-1524
    DOI 10.1091/mbc.E13-11-0658
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Glial precursors clear sensory neuron corpses during development via Jedi-1, an engulfment receptor.

    Wu, Hsiao-Huei / Bellmunt, Elena / Scheib, Jami L / Venegas, Victor / Burkert, Cornelia / Reichardt, Louis F / Zhou, Zheng / Fariñas, Isabel / Carter, Bruce D

    Nature neuroscience

    2009  Volume 12, Issue 12, Page(s) 1534–1541

    Abstract: During the development of peripheral ganglia, 50% of the neurons that are generated undergo apoptosis. How the massive numbers of corpses are removed is unknown. We found that satellite glial cell precursors are the primary phagocytic cells for apoptotic ...

    Abstract During the development of peripheral ganglia, 50% of the neurons that are generated undergo apoptosis. How the massive numbers of corpses are removed is unknown. We found that satellite glial cell precursors are the primary phagocytic cells for apoptotic corpse removal in developing mouse dorsal root ganglia (DRG). Confocal and electron microscopic analysis revealed that glial precursors, rather than macrophages, were responsible for clearing most of the dead DRG neurons. Moreover, we identified Jedi-1, an engulfment receptor, and MEGF10, a purported engulfment receptor, as homologs of the invertebrate engulfment receptors Draper and CED-1 expressed in the glial precursor cells. Expression of Jedi-1 or MEGF10 in fibroblasts facilitated binding to dead neurons, and knocking down either protein in glial cells or overexpressing truncated forms lacking the intracellular domain inhibited engulfment of apoptotic neurons. Together, these results suggest a cellular and molecular mechanism by which neuronal corpses are culled during DRG development.
    MeSH term(s) Animals ; Apoptosis/physiology ; Cells, Cultured ; Female ; Fibroblasts/physiology ; Ganglia, Spinal/cytology ; Ganglia, Spinal/embryology ; Gene Expression Regulation, Developmental ; Green Fluorescent Proteins/genetics ; Humans ; Kidney/cytology ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Mice, Transgenic ; Nerve Growth Factor/pharmacology ; Neuroglia/cytology ; Phagocytosis/physiology ; Pregnancy ; Sensory Receptor Cells/cytology ; Sensory Receptor Cells/drug effects ; Stem Cells/drug effects ; Stem Cells/physiology
    Chemical Substances Jedi protein, mouse ; Megf10 protein, mouse ; Membrane Proteins ; Green Fluorescent Proteins (147336-22-9) ; Nerve Growth Factor (9061-61-4)
    Language English
    Publishing date 2009-11-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1420596-8
    ISSN 1546-1726 ; 1097-6256
    ISSN (online) 1546-1726
    ISSN 1097-6256
    DOI 10.1038/nn.2446
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    Zs.MG 67: Show issues

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  7. Article ; Online: (R)-Profens are substrate-selective inhibitors of endocannabinoid oxygenation by COX-2.

    Duggan, Kelsey C / Hermanson, Daniel J / Musee, Joel / Prusakiewicz, Jeffery J / Scheib, Jami L / Carter, Bruce D / Banerjee, Surajit / Oates, J A / Marnett, Lawrence J

    Nature chemical biology

    2011  Volume 7, Issue 11, Page(s) 803–809

    Abstract: Cyclooxygenase-2 (COX-2) catalyzes the oxygenation of arachidonic acid and the endocannabinoids 2-arachidonoylglycerol and arachidonoylethanolamide. Evaluation of a series of COX-2 inhibitors revealed that many weak competitive inhibitors of arachidonic ... ...

    Abstract Cyclooxygenase-2 (COX-2) catalyzes the oxygenation of arachidonic acid and the endocannabinoids 2-arachidonoylglycerol and arachidonoylethanolamide. Evaluation of a series of COX-2 inhibitors revealed that many weak competitive inhibitors of arachidonic acid oxygenation are potent inhibitors of endocannabinoid oxygenation. (R) enantiomers of ibuprofen, naproxen and flurbiprofen, which are considered to be inactive as COX-2 inhibitors, are potent 'substrate-selective inhibitors' of endocannabinoid oxygenation. Crystal structures of the COX-2–(R)-naproxen and COX-2–(R)-flurbiprofen complexes verified this unexpected binding and defined the orientation of the (R) enantiomers relative to (S) enantiomers. (R)-Profens selectively inhibited endocannabinoid oxygenation by lipopolysaccharide-stimulated dorsal root ganglion (DRG) cells. Substrate-selective inhibition provides new tools for investigating the role of COX-2 in endocannabinoid oxygenation and a possible explanation for the ability of (R)-profens to maintain endocannabinoid tone in models of neuropathic pain.
    MeSH term(s) Arachidonic Acid/metabolism ; Arachidonic Acids/metabolism ; Cannabinoid Receptor Modulators/metabolism ; Catalytic Domain ; Chemistry, Pharmaceutical ; Cyclooxygenase 2/metabolism ; Cyclooxygenase 2 Inhibitors/chemistry ; Cyclooxygenase 2 Inhibitors/pharmacology ; Endocannabinoids ; Glycerides/metabolism ; Models, Molecular ; Oxidation-Reduction ; Protein Binding ; Protein Conformation ; Substrate Specificity
    Chemical Substances Arachidonic Acids ; Cannabinoid Receptor Modulators ; Cyclooxygenase 2 Inhibitors ; Endocannabinoids ; Glycerides ; Arachidonic Acid (27YG812J1I) ; glyceryl 2-arachidonate (8D239QDW64) ; Cyclooxygenase 2 (EC 1.14.99.1)
    Language English
    Publishing date 2011-11-03
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2202962-X
    ISSN 1552-4469 ; 1552-4450
    ISSN (online) 1552-4469
    ISSN 1552-4450
    DOI 10.1038/nchembio.663
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