PUBLICATION

Innate Immune Pathways Promote Oligodendrocyte Progenitor Cell Recruitment to the Injury Site in Adult Zebrafish Brain

Authors
Sanchez-Gonzalez, R., Koupourtidou, C., Lepko, T., Zambusi, A., Novoselc, K.T., Durovic, T., Aschenbroich, S., Schwarz, V., Breunig, C.T., Straka, H., Huttner, H.B., Irmler, M., Beckers, J., Wurst, W., Zwergal, A., Schauer, T., Straub, T., Czopka, T., Trümbach, D., Götz, M., Stricker, S.H., Ninkovic, J.
ID
ZDB-PUB-220216-7
Date
2022
Source
Cells   11(3): (Journal)
Registered Authors
Czopka, Tim
Keywords
brain injury, brain regeneration, innate immunity pathways, neurogenesis, oligodendrocyte progenitors, reactive gliosis, zebrafish
Datasets
GEO:GSE98217
MeSH Terms
  • Animals
  • Brain
  • Gliosis/metabolism
  • Immunity, Innate
  • Oligodendrocyte Precursor Cells*/metabolism
  • Zebrafish
PubMed
35159329 Full text @ Cells
Abstract
The oligodendrocyte progenitors (OPCs) are at the front of the glial reaction to the traumatic brain injury. However, regulatory pathways steering the OPC reaction as well as the role of reactive OPCs remain largely unknown. Here, we compared a long-lasting, exacerbated reaction of OPCs to the adult zebrafish brain injury with a timely restricted OPC activation to identify the specific molecular mechanisms regulating OPC reactivity and their contribution to regeneration. We demonstrated that the influx of the cerebrospinal fluid into the brain parenchyma after injury simultaneously activates the toll-like receptor 2 (Tlr2) and the chemokine receptor 3 (Cxcr3) innate immunity pathways, leading to increased OPC proliferation and thereby exacerbated glial reactivity. These pathways were critical for long-lasting OPC accumulation even after the ablation of microglia and infiltrating monocytes. Importantly, interference with the Tlr1/2 and Cxcr3 pathways after injury alleviated reactive gliosis, increased new neuron recruitment, and improved tissue restoration.
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