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@ARTICLE{Stokowska:1007674,
      author       = {Stokowska, Anna and Aswendt, Markus and Zucha, Daniel and
                      Lohmann, Stephanie and Wieters, Frederique and Morán
                      Suarez, Javier and Atkins, Alison L. and Li, YiXian and
                      Miteva, Maria and Lewin, Julia and Wiedermann, Dirk and
                      Diedenhofen, Michael and Torinsson Naluai, Åsa and Abaffy,
                      Pavel and Valihrach, Lukas and Kubista, Mikael and Hoehn,
                      Mathias and Pekny, Milos and Pekna, Marcela},
      title        = {{C}omplement {C}3a treatment accelerates recovery after
                      stroke via modulation of astrocyte reactivity and cortical
                      connectivity},
      journal      = {The journal of clinical investigation},
      volume       = {133},
      number       = {10},
      issn         = {0021-9738},
      address      = {Ann Arbor, Mich.},
      publisher    = {ASCJ},
      reportid     = {FZJ-2023-02157},
      pages        = {e162253},
      year         = {2023},
      abstract     = {Despite advances in acute care, ischemic stroke remains a
                      major cause of long-term disability. Approaches targeting
                      both neuronal and glial responses are needed to enhance
                      recovery and improve long-term outcome. The complement C3a
                      receptor (C3aR) is a regulator of inflammation with roles in
                      neurodevelopment, neural plasticity, and neurodegeneration.
                      Using mice lacking C3aR (C3aR–/–) and mice
                      overexpressing C3a in the brain, we uncovered 2 opposing
                      effects of C3aR signaling on functional recovery after
                      ischemic stroke: inhibition in the acute phase and
                      facilitation in the later phase. Peri-infarct astrocyte
                      reactivity was increased and density of microglia reduced in
                      C3aR–/– mice; C3a overexpression led to the opposite
                      effects. Pharmacological treatment of wild-type mice with
                      intranasal C3a starting 7 days after stroke accelerated
                      recovery of motor function and attenuated astrocyte
                      reactivity without enhancing microgliosis. C3a treatment
                      stimulated global white matter reorganization, increased
                      peri-infarct structural connectivity, and upregulated Igf1
                      and Thbs4 in the peri-infarct cortex. Thus, C3a treatment
                      from day 7 after stroke exerts positive effects on
                      astrocytes and neuronal connectivity while avoiding the
                      deleterious consequences of C3aR signaling during the acute
                      phase. Intranasal administration of C3aR agonists within a
                      convenient time window holds translational promise to
                      improve outcome after ischemic stroke.},
      cin          = {INM-3},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-3-20090406},
      pnm          = {5251 - Multilevel Brain Organization and Variability
                      (POF4-525) / DFG project 431549029 - SFB 1451:
                      Schlüsselmechanismen normaler und krankheitsbedingt
                      gestörter motorischer Kontrolle (431549029)},
      pid          = {G:(DE-HGF)POF4-5251 / G:(GEPRIS)431549029},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {36995772},
      UT           = {WOS:000998153000004},
      doi          = {10.1172/JCI162253},
      url          = {https://juser.fz-juelich.de/record/1007674},
}