Complement: A novel factor in basal and ischemia-induced neurogenesis

Yalda Rahpeymai, Max Albert Hietala, Ulrika Wilhelmsson, Andrew Fotheringham, Ioan Davies, Ann Katrin Nilsson, Jörg Zwirner, Rick A. Wetsel, Craig Gerard, Milos Pekny, Marcela Pekna

    Research output: Contribution to journalArticlepeer-review

    Abstract

    Through its involvement in inflammation, opsonization, and cytolysis, the complement protects against infectious agents. Although most of the complement proteins are synthesized in the central nervous system (CNS), the role of the complement system in the normal or ischemic CNS remains unclear. Here we demonstrate for the first time that neural progenitor cells and immature neurons express receptors for complement fragments C3a and C5a (C3a receptor (C3aR) and C5a receptor). Mice that are deficient in complement factor C3 (C3 -/-) lack C3a and are unable to generate C5a through proteolytic cleavage of C5 by C5-convertase. Intriguingly, basal neurogenesis is decreased both in C3-/- mice and in mice lacking C3aR or mice treated with a C3aR antagonist. The C3-/- mice had impaired ischemia-induced neurogenesis both in the subventricular zone, the main source of neural progenitor cells in adult brain, and in the ischemic region, despite normal proliferative response and larger infarct volumes. Thus, in the adult mammalian CNS, complement activation products promote both basal and ischemia-induced neurogenesis. © 2006 European Molecular Biology Organization | All Rights Reserved.
    Original languageEnglish
    Pages (from-to)1364-1374
    Number of pages10
    JournalEMBO Journal
    Volume25
    Issue number6
    DOIs
    Publication statusPublished - 22 Mar 2006

    Keywords

    • C3
    • Cerebral ischemia
    • Complement system
    • Mice
    • Neurogenesis

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