title: Signaling through C5aR is not involved in basal neurogenesis.
abstract: The complement system, an important part of the innate immune system, provides protection against invading pathogens, in part through its proinflammatory activities. Although most complement proteins are synthesized locally in the brain and the relevant complement receptors are expressed on resident brain cells, little is known about brain-specific role(s) of the complement system. C3a and C5a, complement-derived peptides with anaphylatoxic properties, have been implicated in noninflammatory functions, such as tissue regeneration and neuroprotection. Recently, we have shown that signaling through C3a receptor (C3aR) is involved in the regulation of neurogenesis. In the present study, we assessed basal neurogenesis in mice lacking C5a receptor (C5aR(-/-)) and mice expressing C3a and C5a, respectively in the CNS under the control of glial fibrillary acidic protein (GFAP) promoter (C3a/GFAP and C5a/GFAP, respectively) and thus without the requirement for complement activation. We did not observe any difference among C5aR(-/-), C3a/GFAP and C5a/GFAP mice and their respective controls in the number of newly formed neuroblasts and newly formed neurons in the subventricular zone (SVZ) of lateral ventricles and hippocampal dentate gyrus, the two neurogenic niches in the adult brain, or the olfactory bulb, the final destination of new neurons formed in the SVZ. Our results indicate that signaling through C5aR is not involved in basal neurogenesis in adult mice and that basal neurogenesis in adult C3a/GFAP and C5a/GFAP mice is not altered.
authors.affiliation: Department of Medical Chemistry and Cell Biology, Institute of Biomedicine, Sahlgrenska Academy at Göteborg University, Göteborg, Sweden.
authors.forename: Yalda Rahpeymai
authors.initials: YR
authors.lastname: Bogestål
authors.forename: Scott R
authors.initials: SR
authors.lastname: Barnum
authors.forename: Peter L P
authors.initials: PL
authors.lastname: Smith
authors.forename: Victor
authors.initials: V
authors.lastname: Mattisson
authors.forename: Milos
authors.initials: M
authors.lastname: Pekny
authors.forename: Marcela
authors.initials: M
authors.lastname: Pekna
mesh_terms: D000818:Animals; D001973:Bromodeoxyuridine / Q000378:metabolism; D002452:Cell Count / Q000379:methods; D049109:Cell Proliferation; D015926:Complement C3a / Q000235:genetics; D015936:Complement C5a / Q000235:genetics; D000089622:Doublecortin Domain Proteins; D005904:Glial Fibrillary Acidic Protein / Q000096:biosynthesis; D020547:Lateral Ventricles / Q000166:cytology*; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D009474:Neurons / Q000502:physiology*; D009479:Neuropeptides / Q000378:metabolism; D010751:Phosphopyruvate Hydratase / Q000378:metabolism; D044087:Receptor, Anaphylatoxin C5a / Q000172:deficiency / Q000502:physiology*; D015398:Signal Transduction / Q000235:genetics / Q000502:physiology*
chemical_list: D000089622:Doublecortin Domain Proteins; D005904:Glial Fibrillary Acidic Protein; D008869:Microtubule-Associated Proteins; D009479:Neuropeptides; D044087:Receptor, Anaphylatoxin C5a; D015926:Complement C3a; D015936:Complement C5a; D010751:Phosphopyruvate Hydratase; D001973:Bromodeoxyuridine