ArticleMolecular neurobiology2016
Complement Peptide C3a Promotes Astrocyte Survival in Response to Ischemic Stress.
Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 45 citations in OpenAlex.
- Curing the brain: in search for new astrocyte-specific therapies.Experimental & molecular medicine · 2026Review
- Review
- Lipidomic and proteomic insights from extracellular vesicles in the postmortem dorsolateral prefrontal cortex reveal substance use disorder-induced brain changes.Translational psychiatry · 2025Article
- Stroke and Neurogenesis: Bridging Clinical Observations to New Mechanistic Insights from Animal Models.Translational stroke research · 2024Review
- Complement C3a treatment accelerates recovery after stroke via modulation of astrocyte reactivity and cortical connectivity.The Journal of clinical investigation · 2023Article
- Astrocyte Responses to Complement Peptide C3a are Highly Context-Dependent.Neurochemical research · 2023Article
- Complement C3a activates astrocytes to promote medulloblastoma progression through TNF-α.Journal of neuroinflammation · 2022Article
- Targeting Complement C3a Receptor to Improve Outcome After Ischemic Brain Injury.Neurochemical research · 2021Review
- Review
- Astrocyte Activation in Neurovascular Damage and Repair Following Ischaemic Stroke.International journal of molecular sciences · 2021Review
- 4R-cembranoid confers neuroprotection against LPS-induced hippocampal inflammation in mice.Journal of neuroinflammation · 2021Article
- C3a Receptor Signaling Inhibits Neurodegeneration Induced by Neonatal Hypoxic-Ischemic Brain Injury.Frontiers in immunology · 2021Article
- Hyperactive Behavior and Altered Brain Morphology in Adult Complement C3a Receptor Deficient Mice.Frontiers in immunology · 2021Article
- Sustained activation of C3aR in a human podocyte line impairs the morphological maturation of the cells.Molecular medicine reports · 2020Article
- The good, the bad, and the opportunities of the complement system in neurodegenerative disease.Journal of neuroinflammation · 2020Review
- Glial Cells: Role of the Immune Response in Ischemic Stroke.Frontiers in immunology · 2020Review
- Article
- The complement system in schizophrenia: where are we now and what's next?Molecular psychiatry · 2020Review
- Article
- Significance of Complement System in Ischemic Stroke: A Comprehensive Review.Aging and disease · 2019Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Astrocytes are the most numerous cells in the central nervous system with a range of homeostatic and regulatory functions. Under normal conditions as well as after ischemia, astrocytes promote neuronal survival. We have previously reported that the complement-derived peptide C3a stimulates neuronal differentiation of neural progenitor cells and protects the immature brain tissue against hypoxic-ischemic injury. Here, we studied the effects of C3a on the response of mouse cortical astrocytes to ischemia. We have found that chemical ischemia, induced by combined inhibition of oxidative phosphorylation and glycolysis, upregulates the expression of C3a receptor in cultured primary astrocytes. C3a treatment protected wild-type but not C3a receptor-deficient astrocytes from cell death induced by chemical ischemia or oxygen-glucose deprivation by reducing ERK signaling and caspase-3 activation. C3a attenuated ischemia-induced upregulation of glial fibrillary acidic protein; however, the protective effects of C3a were not dependent on the presence of the astrocyte intermediate filament system. Pre-treatment of astrocytes with C3a during recovery abrogated the ischemia-induced neuroprotective phenotype of astrocytes. Jointly, these results provide the first evidence that the complement peptide C3a modulates the response of astrocytes to ischemia and increases their ability to cope with ischemic stress.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.