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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HI_Neurodegenration_C3aR

Source data for findings reported in paper "C3a receptor signaling inhibits neurodegeneration induced by neonatal hypoxic-ischemic brain injury", Pozo-Rodrigalvarez et al..

authors: -

firstname: Andrea
lastname: Pozo-Rodrigalvarez
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'

firstname: Yixian
lastname: Li
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'

firstname: Jingyun
lastname: Wu
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'

firstname: Verena
lastname: Dehm
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'

firstname: Anna
lastname: Stokowska
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'
id: 'ORCID:0000-0001-5237-3341'

firstname: Hanna
lastname: Sourkova
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'

firstname: Harry
lastname: Steinbusch
affiliation: 'Department of Neuroscience, Faculty of Health, Medicine and Life Sciences, Maastricht University, The Netherlands'

firstname: Carina
lastname: Mallard
affiliation: 'Centre of Perinatal Medicine & Health, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden'

firstname: Henrik
lastname: Hagberg
affiliation: 'Centre of Perinatal Medicine & Health, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden'

firstname: Milos
lastname: Pekny
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'
id: 'ORCID:0000-0003-1607-8075'

firstname: Marcela
lastname: Pekna
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'
id: 'ORCID:0000-0003-2734-8237'

title: 'C3a receptor signaling inhibits neurodegeneration induced by neonatal hypoxic-ischemic brain injury' 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" keywords:

'Neonatal encephalopathy'
'Developing brain'
Nypoxia-ischemia
Neurodegeneration
'Reactive gliosis'
Neuroscience license: name: 'Creative Commons CC0 1.0 Public Domain Dedication' url: 'https://creativecommons.org/publicdomain/zero/1.0/' funding: [] references: [] resourcetype: Dataset templateversion: 1.2

datacite.yml
Title	C3a receptor signaling inhibits neurodegeneration induced by neonatal hypoxic-ischemic brain injury
Authors	Pozo-Rodrigalvarez,Andrea;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 Li,Yixian;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 Wu,Jingyun;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 Dehm,Verena;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 Stokowska,Anna;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;ORCID:0000-0001-5237-3341 Sourkova,Hanna;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 Steinbusch,Harry;Department of Neuroscience, Faculty of Health, Medicine and Life Sciences, Maastricht University, The Netherlands Mallard,Carina;Centre of Perinatal Medicine & Health, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden Hagberg,Henrik;Centre of Perinatal Medicine & Health, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden Pekny,Milos;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;ORCID:0000-0003-1607-8075 Pekna,Marcela;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;ORCID:0000-0003-2734-8237
Description	Hypoxic-ischemic neonatal encephalopathy due to perinatal asphyxia is the leading cause of brain injury in newborns. Clinical data suggest that brain inflammation induced by perinatal insults can persist for years. We previously showed that signaling through the receptor for complement peptide C3a (C3aR) protects against cognitive impairment induced by experimental perinatal asphyxia. To investigate the long-term neuropathological effects of hypoxic-ischemic injury to the developing brain and the role of C3aR signaling therein, we subjected wildtype mice, C3aR deficient mice, and mice expressing biologically active C3a in the CNS to mild hypoxic-ischemic brain injury on postnatal day 9. We found that such injury triggers neurodegeneration and pronounced reactive gliosis in the ipsilesional hippocampus both of which persist long into adulthood. Transgenic expression of C3a in reactive astrocytes reduced hippocampal neurodegeneration and reactive gliosis. In contrast, neurodegeneration and microglial cell density increased in mice lacking C3aR. Intranasal administration of C3a for 3 days starting 1 h after induction of hypoxia-ischemia reduced neurodegeneration and reactive gliosis in the hippocampus of wildtype mice. We conclude that neonatal hypoxic-ischemic brain injury leads to long-lasting neurodegeneration. This neurodegeneration is substantially reduced by treatment with C3aR agonists, conceivably through modulation of reactive gliosis.
License	Creative Commons CC0 1.0 Public Domain Dedication (https://creativecommons.org/publicdomain/zero/1.0/)
References
Funding
Keywords	Neonatal encephalopathy Developing brain Nypoxia-ischemia Neurodegeneration Reactive gliosis Neuroscience
Resource Type	Dataset

README.md

HI_Neurodegenration_C3aR