ArticleFrontiers in immunology2021
C3a Receptor Signaling Inhibits Neurodegeneration Induced by Neonatal Hypoxic-Ischemic Brain Injury.
Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.
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14 citing papers in PubMed, 21 citations in OpenAlex.
- Intranasal therapies for neonatal hypoxic-ischemic encephalopathy.Neural regeneration research · 2026Article
- Human chorionic gonadotropin decreases cerebral cystic encephalomalacia and parvalbumin interneuron degeneration in a pro-inflammatory model of mouse neonatal hypoxia-ischemia.Scientific reports · 2026Article
- CXCR3 Deficiency Alleviates Retinal Ganglion Cell Loss by Regulating Neuron-Astrocyte Communication in a Mouse Model of Glaucoma.Investigative ophthalmology & visual science · 2025Article
- Review
- The Impact of the Histone Deacetylase Inhibitor-Sodium Butyrate on Complement-Mediated Synapse Loss in a Rat Model of Neonatal Hypoxia-Ischemia.Molecular neurobiology · 2025Article
- Structural and Functional Effects of C5aR1 Antagonism in a Rat Model of Neonatal Hypoxic-Ischemic Encephalopathy.Developmental neuroscience · 2025Article
- Extracellular vesicles: biological mechanisms and emerging therapeutic opportunities in neurodegenerative diseases.Translational neurodegeneration · 2024Review
- The post-stroke young adult brain has limited capacity to re-express the gene expression patterns seen during early postnatal brain development.Brain pathology (Zurich, Switzerland) · 2024Article
- Hypoxia-induced complement component 3 promotes aggressive tumor growth in the glioblastoma microenvironment.JCI insight · 2024Article
- Review
- Moss-produced human complement factor H with modified glycans has an extended half-life and improved biological activity.Frontiers in immunology · 2024Article
- A role for P-selectin and complement in the pathological sequelae of germinal matrix hemorrhage.Journal of neuroinflammation · 2023Article
- Astrocyte Responses to Complement Peptide C3a are Highly Context-Dependent.Neurochemical research · 2023Article
- A Role for P-selectin and Complement in the Pathological Sequelae of Germinal Matrix Hemorrhage.Research square · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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