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@ARTICLE{Nespoli:267348,
author = {Nespoli, Ester and Hakani, Marsela and Hein, Tabea Melissa
and May, Stephanie Nadine and Danzer, Karin and Wirth,
Thomas and Baumann, Bernd and Dimou, Leda},
title = {{G}lial cells react to closed head injury in a distinct and
spatiotemporally orchestrated manner.},
journal = {Scientific reports},
volume = {14},
number = {1},
issn = {2045-2322},
address = {[London]},
publisher = {Macmillan Publishers Limited, part of Springer Nature},
reportid = {DZNE-2024-00112},
pages = {2441},
year = {2024},
abstract = {Traumatic brain injury (TBI) is a leading cause of
mortality and disability worldwide. Acute neuroinflammation
is a prominent reaction after TBI and is mostly initiated by
brain-resident glial cells such as microglia, NG2-glia and
astrocytes. The magnitude of this reaction paves the way for
long-lasting consequences such as chronic neurological
pathologies, for which therapeutic options remain limited.
The neuroinflammatory response to TBI is mostly studied with
craniotomy-based animal models that are very robust but also
rather artificial. Here, we aimed to analyze the reaction of
glial cells in a highly translational but variable closed
head injury (CHI) model and were able to correlate the
severity of the trauma to the degree of glial response.
Furthermore, we could show that the different glial cell
types react in a temporally and spatially orchestrated
manner in terms of morphological changes, proliferation, and
cell numbers in the first 15 days after the lesion.
Interestingly, NG2-glia, the only proliferating cells in the
healthy brain parenchyma, divided at a rate that was
correlated with the size of the injury. Our findings
describe the previously uncharacterized posttraumatic
response of the major brain glial cell types in CHI in order
to gain a detailed understanding of the course of
neuroinflammatory events; such knowledge may open novel
avenues for future therapeutic approaches in TBI.},
keywords = {Animals / Neuroglia: metabolism / Brain: metabolism / Brain
Injuries, Traumatic: pathology / Astrocytes: metabolism /
Microglia: metabolism / Head Injuries, Closed: pathology /
Disease Models, Animal},
cin = {AG Danzer},
ddc = {600},
cid = {I:(DE-2719)5000072},
pnm = {352 - Disease Mechanisms (POF4-352)},
pid = {G:(DE-HGF)POF4-352},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:38286816},
pmc = {pmc:PMC10825139},
doi = {10.1038/s41598-024-52337-4},
url = {https://pub.dzne.de/record/267348},
}