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@@ -1,3 +1,68 @@
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# HI_Neurodegenration_C3aR
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-Source data for findings reported in paper "C3a receptor signaling inhibits neurodegeneration induced by neonatal hypoxic-ischemic brain injury", Pozo-Rodrigalvarez et al..
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+Source data for findings reported in paper "C3a receptor signaling inhibits neurodegeneration induced by neonatal hypoxic-ischemic brain injury", Pozo-Rodrigalvarez et al..
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+
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+authors:
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+ -
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+ firstname: Andrea
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+ lastname: Pozo-Rodrigalvarez
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+ affiliation: 'Laboratory of Regenerative Neuroimmunology, Center for Brain Repair, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden'
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+ -
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+ firstname: Yixian
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+ lastname: Li
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+ affiliation: 'Laboratory of Regenerative Neuroimmunology, Center for Brain Repair, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden'
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+ -
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+ firstname: Jingyun
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+ lastname: Wu
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+ affiliation: 'Laboratory of Regenerative Neuroimmunology, Center for Brain Repair, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden'
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+ -
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+ firstname: Verena
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+ lastname: Dehm
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+ affiliation: 'Laboratory of Regenerative Neuroimmunology, Center for Brain Repair, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden'
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+ -
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+ firstname: Anna
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+ lastname: Stokowska
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+ affiliation: 'Laboratory of Regenerative Neuroimmunology, Center for Brain Repair, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden'
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+ id: 'ORCID:0000-0001-5237-3341'
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+ -
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+ firstname: Hanna
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+ lastname: Sourkova
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+ affiliation: 'Laboratory of Astrocyte Biology and CNS Regeneration, Center for Brain Repair, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden'
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+ -
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+ firstname: Harry
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+ lastname: Steinbusch
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+ affiliation: 'Department of Neuroscience, Faculty of Health, Medicine and Life Sciences, Maastricht University, The Netherlands'
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+ -
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+ firstname: Carina
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+ lastname: Mallard
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+ affiliation: 'Centre of Perinatal Medicine & Health, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden'
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+ -
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+ firstname: Henrik
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+ lastname: Hagberg
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+ affiliation: 'Centre of Perinatal Medicine & Health, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden'
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+ -
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+ firstname: Milos
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+ lastname: Pekny
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+ affiliation: 'Laboratory of Astrocyte Biology and CNS Regeneration, Center for Brain Repair, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden'
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+ id: 'ORCID:0000-0003-1607-8075'
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+ -
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+ firstname: Marcela
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+ lastname: Pekna
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+ affiliation: 'Laboratory of Regenerative Neuroimmunology, Center for Brain Repair, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Swede'
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+ id: 'ORCID:0000-0003-2734-8237'
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+title: 'C3a receptor signaling inhibits neurodegeneration induced by neonatal hypoxic-ischemic brain injury'
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+description: "Hypoxic-ischemic neonatal encephalopathy due to perinatal asphyxia is the leading cause of brain injury \n in newborns. Clinical data suggest that brain inflammation induced by perinatal insults can persist for \n years. We previously showed that signaling through the receptor for complement peptide C3a (C3aR) \n protects against cognitive impairment induced by experimental perinatal asphyxia. To investigate the \n long-term neuropathological effects of hypoxic-ischemic injury to the developing brain and the role \n of C3aR signaling therein, we subjected wildtype mice, C3aR deficient mice, and mice expressing \n biologically active C3a in the CNS to mild hypoxic-ischemic brain injury on postnatal day 9. We found \n that such injury triggers neurodegeneration and pronounced reactive gliosis in the ipsilesional \n hippocampus both of which persist long into adulthood. Transgenic expression of C3a in reactive astrocytes\n reduced hippocampal neurodegeneration and reactive gliosis. In contrast, neurodegeneration and microglial \n cell density increased in mice lacking C3aR. Intranasal administration of C3a for 3 days starting \n 1 h after induction of hypoxia-ischemia reduced neurodegeneration and reactive gliosis in the hippocampus\n of wildtype mice. We conclude that neonatal hypoxic-ischemic brain injury leads to long-lasting \n neurodegeneration. This neurodegeneration is substantially reduced by treatment with C3aR agonists, \n conceivably through modulation of reactive gliosis.\n"
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+keywords:
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+ - 'Neonatal encephalopathy'
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+ - 'Developing brain'
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+ - Nypoxia-ischemia
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+ - Neurodegeneration
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+ - 'Reactive gliosis'
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+ - Neuroscience
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+license:
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+ name: 'Creative Commons CC0 1.0 Public Domain Dedication'
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+ url: 'https://creativecommons.org/publicdomain/zero/1.0/'
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+funding: []
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+references: []
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+resourcetype: Dataset
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+templateversion: 1.2
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