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  • 1
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    CNS synaptogenesis promoted by glia-derived cholesterol (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-11-10
    Description: The molecular mechanisms controlling synaptogenesis in the central nervous system (CNS) are poorly understood. Previous reports showed that a glia-derived factor strongly promotes synapse development in cultures of purified CNS neurons. Here, we identify this factor as cholesterol complexed to apolipoprotein E-containing lipoproteins. CNS neurons produce enough cholesterol to survive and grow, but the formation of numerous mature synapses demands additional amounts that must be provided by glia. Thus, the availability of cholesterol appears to limit synapse development. This may explain the delayed onset of CNS synaptogenesis after glia differentiation and neurobehavioral manifestations of defects in cholesterol or lipoprotein homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mauch, D H -- Nagler, K -- Schumacher, S -- Goritz, C -- Muller, E C -- Otto, A -- Pfrieger, F W -- New York, N.Y. -- Science. 2001 Nov 9;294(5545):1354-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Synapse Group and, Protein Chemistry Group, Max-Delbruck-Center for Molecular Medicine, D-13092 Berlin, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11701931" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anticholesteremic Agents/pharmacology ; Apolipoproteins E/metabolism ; Cells, Cultured ; Cholesterol/*metabolism/pharmacology ; Culture Media, Conditioned ; Excitatory Postsynaptic Potentials ; Lovastatin/*analogs & derivatives/pharmacology ; Neuroglia/*metabolism ; Patch-Clamp Techniques ; Phosphatidylcholines/pharmacology ; Rats ; Rats, Sprague-Dawley ; Retinal Ganglion Cells/metabolism/*physiology ; Sphingomyelins/pharmacology ; Synapses/drug effects/*physiology ; Synaptic Transmission
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Resident neural stem cells restrict tissue damage and neuronal loss after spinal cord injury in mice (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-11-02
    Description: Central nervous system injuries are accompanied by scar formation. It has been difficult to delineate the precise role of the scar, as it is made by several different cell types, which may limit the damage but also inhibit axonal regrowth. We show that scarring by neural stem cell-derived astrocytes is required to restrict secondary enlargement of the lesion and further axonal loss after spinal cord injury. Moreover, neural stem cell progeny exerts a neurotrophic effect required for survival of neurons adjacent to the lesion. One distinct component of the glial scar, deriving from resident neural stem cells, is required for maintaining the integrity of the injured spinal cord.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sabelstrom, Hanna -- Stenudd, Moa -- Reu, Pedro -- Dias, David O -- Elfineh, Marta -- Zdunek, Sofia -- Damberg, Peter -- Goritz, Christian -- Frisen, Jonas -- New York, N.Y. -- Science. 2013 Nov 1;342(6158):637-40. doi: 10.1126/science.1242576.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Molecular Biology, Karolinska Institute, SE-171 77 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24179227" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Astrocytes/physiology ; Axons/*physiology ; Cell Survival ; Cicatrix/*pathology ; Forkhead Transcription Factors/genetics ; Genes, ras ; Mice ; Mice, Mutant Strains ; Neural Stem Cells/*physiology ; Spinal Cord Injuries/*pathology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    A pericyte origin of spinal cord scar tissue (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-07-09
    Description: There is limited regeneration of lost tissue after central nervous system injury, and the lesion is sealed with a scar. The role of the scar, which often is referred to as the glial scar because of its abundance of astrocytes, is complex and has been discussed for more than a century. Here we show that a specific pericyte subtype gives rise to scar-forming stromal cells, which outnumber astrocytes, in the injured spinal cord. Blocking the generation of progeny by this pericyte subtype results in failure to seal the injured tissue. The formation of connective tissue is common to many injuries and pathologies, and here we demonstrate a cellular origin of fibrosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goritz, Christian -- Dias, David O -- Tomilin, Nikolay -- Barbacid, Mariano -- Shupliakov, Oleg -- Frisen, Jonas -- 250297/European Research Council/International -- New York, N.Y. -- Science. 2011 Jul 8;333(6039):238-42. doi: 10.1126/science.1203165.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Molecular Biology, Karolinska Institute, Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21737741" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/pathology/physiology ; Blood Vessels/pathology ; Cell Count ; Cell Proliferation ; Cicatrix/*pathology ; Fibrosis ; Mice ; Mice, Transgenic ; Pericytes/*pathology/physiology ; Spinal Cord/blood supply/*pathology ; Spinal Cord Injuries/*pathology ; Stromal Cells/pathology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    A latent neurogenic program in astrocytes regulated by Notch signaling in the mouse (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-10-11
    Description: Neurogenesis is restricted in the adult mammalian brain; most neurons are neither exchanged during normal life nor replaced in pathological situations. We report that stroke elicits a latent neurogenic program in striatal astrocytes in mice. Notch1 signaling is reduced in astrocytes after stroke, and attenuated Notch1 signaling is necessary for neurogenesis by striatal astrocytes. Blocking Notch signaling triggers astrocytes in the striatum and the medial cortex to enter a neurogenic program, even in the absence of stroke, resulting in 850 +/- 210 (mean +/- SEM) new neurons in a mouse striatum. Thus, under Notch signaling regulation, astrocytes in the adult mouse brain parenchyma carry a latent neurogenic program that may potentially be useful for neuronal replacement strategies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Magnusson, Jens P -- Goritz, Christian -- Tatarishvili, Jemal -- Dias, David O -- Smith, Emma M K -- Lindvall, Olle -- Kokaia, Zaal -- Frisen, Jonas -- New York, N.Y. -- Science. 2014 Oct 10;346(6206):237-41. doi: 10.1126/science.346.6206.237. Epub 2014 Oct 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Molecular Biology, Karolinska Institute, SE-171 77 Stockholm, Sweden. ; Lund Stem Cell Center, University Hospital, SE-221 84 Lund, Sweden. ; Division of Translational Cancer Research, Lund University, SE-223 63 Lund, Sweden. ; Department of Cell and Molecular Biology, Karolinska Institute, SE-171 77 Stockholm, Sweden. jonas.frisen@ki.se.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25301628" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/cytology/*physiology ; Corpus Striatum/pathology/physiopathology ; Gene Deletion ; Immunoglobulin J Recombination Signal Sequence-Binding Protein/genetics ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neural Stem Cells/cytology/*physiology ; Neurogenesis/genetics/*physiology ; Neurons/cytology/*physiology ; Receptor, Notch1/genetics/*physiology ; *Signal Transduction ; Stroke/pathology/*physiopathology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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