PUBLICATION

TDP-43 condensates and lipid droplets regulate the reactivity of microglia and regeneration after traumatic brain injury

Authors
Zambusi, A., Novoselc, K.T., Hutten, S., Kalpazidou, S., Koupourtidou, C., Schieweck, R., Aschenbroich, S., Silva, L., Yazgili, A.S., van Bebber, F., Schmid, B., Möller, G., Tritscher, C., Stigloher, C., Delbridge, C., Sirko, S., Günes, Z.I., Liebscher, S., Schlegel, J., Aliee, H., Theis, F., Meiners, S., Kiebler, M., Dormann, D., Ninkovic, J.
ID
ZDB-PUB-221125-17
Date
2022
Source
Nature Neuroscience   25(12): 1608-1625 (Journal)
Registered Authors
Ninkovic, Jovica, Schmid, Bettina, Stigloher, Christian, van Bebber, Frauke
Keywords
none
Datasets
GEO:GSE179134
MeSH Terms
  • Animals
  • Brain Injuries, Traumatic*
  • DNA-Binding Proteins
  • Humans
  • Lipid Droplets
  • Microglia*
  • Regeneration
  • Zebrafish
PubMed
36424432 Full text @ Nat. Neurosci.
Abstract
Decreasing the activation of pathology-activated microglia is crucial to prevent chronic inflammation and tissue scarring. In this study, we used a stab wound injury model in zebrafish and identified an injury-induced microglial state characterized by the accumulation of lipid droplets and TAR DNA-binding protein of 43 kDa (TDP-43)+ condensates. Granulin-mediated clearance of both lipid droplets and TDP-43+ condensates was necessary and sufficient to promote the return of microglia back to the basal state and achieve scarless regeneration. Moreover, in postmortem cortical brain tissues from patients with traumatic brain injury, the extent of microglial activation correlated with the accumulation of lipid droplets and TDP-43+ condensates. Together, our results reveal a mechanism required for restoring microglia to a nonactivated state after injury, which has potential for new therapeutic applications in humans.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping