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Complement peptide C3a stimulates neural plasticity after experimental brain ischaemia.

Artikel i vetenskaplig tidskrift
Författare Anna Stokowska
Alison L Atkins
Javier Morán
Tulen Pekny
Linda Bulmer
Michaela C. Pascoe
Scott R Barnum
Rick A Wetsel
Jonas A Nilsson
Mike Dragunow
Marcela Pekna
Publicerad i Brain
Volym 140
Nummer/häfte Pt 2
Sidor 353-369
ISSN 0006-8950
Publiceringsår 2017
Publicerad vid Institutionen för kliniska vetenskaper, sektionen för kirurgi och kirurgisk gastroforskning, Avdelningen för kirurgi
Sahlgrenska Cancer Center
Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap
Sidor 353-369
Språk en
Länkar dx.doi.org/10.1093/brain/aww314
Ämneskategorier Neurovetenskap, Neurobiologi


Ischaemic stroke induces endogenous repair processes that include proliferation and differentiation of neural stem cells and extensive rewiring of the remaining neural connections, yet about 50% of stroke survivors live with severe long-term disability. There is an unmet need for drug therapies to improve recovery by promoting brain plasticity in the subacute to chronic phase after ischaemic stroke. We previously showed that complement-derived peptide C3a regulates neural progenitor cell migration and differentiation in vitro and that C3a receptor signalling stimulates neurogenesis in unchallenged adult mice. To determine the role of C3a-C3a receptor signalling in ischaemia-induced neural plasticity, we subjected C3a receptor-deficient mice, GFAP-C3a transgenic mice expressing biologically active C3a in the central nervous system, and their respective wild-type controls to photothrombotic stroke. We found that C3a overexpression increased, whereas C3a receptor deficiency decreased post-stroke expression of GAP43 (P < 0.01), a marker of axonal sprouting and plasticity, in the peri-infarct cortex. To verify the translational potential of these findings, we used a pharmacological approach. Daily intranasal treatment of wild-type mice with C3a beginning 7 days after stroke induction robustly increased synaptic density (P < 0.01) and expression of GAP43 in peri-infarct cortex (P < 0.05). Importantly, the C3a treatment led to faster and more complete recovery of forepaw motor function (P < 0.05). We conclude that C3a-C3a receptor signalling stimulates post-ischaemic neural plasticity and intranasal treatment with C3a receptor agonists is an attractive approach to improve functional recovery after ischaemic brain injury.

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