% IMPORTANT: The following is UTF-8 encoded. This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.
@ARTICLE{Kikhia:281354,
author = {Kikhia, Majed and Schilling, Simone and Herzog,
Marie-Louise and Livne, Michelle and Semtner, Marcus and
Tay, Tuan Leng and Prinz, Marco and Kettenmann, Helmut and
Endres, Matthias and Kronenberg, Golo and Göttert, Ria and
Gertz, Karen},
title = {{M}ulticolor fate mapping of microglia reveals polyclonal
proliferation, heterogeneity, and cell-cell interactions
after ischemic stroke in mice.},
journal = {Nature Communications},
volume = {16},
number = {1},
issn = {2041-1723},
address = {[London]},
publisher = {Springer Nature},
reportid = {DZNE-2025-01101},
pages = {8294},
year = {2025},
abstract = {Microglial proliferation is a principal element of the
inflammatory response to brain ischemia. However, the
precise proliferation dynamics, phenotype acquisition, and
functional consequences of newly emerging microglia are not
yet understood. Using multicolor fate mapping and
computational methods, we here demonstrate that microglia
exhibit polyclonal proliferation in the ischemic lesion of
female mice. The peak number of clones occurs at 14 days,
while the largest clones are observed at 4 weeks
post-stroke. Whole-cell patch-clamp recordings of microglia
reveal a homogeneous acute response to ischemia with a
pattern of outward and inward currents that evolves over
time. In the resolution phase, 8 weeks post-stroke,
microglial cells within one clone share similar membrane
properties, while neighboring microglia from different
clones display more heterogeneous electrophysiological
profiles. Super-resolution microscopy and live-cell imaging
unmask various forms of cell-cell interactions between
microglial cells from different clones. Overall, this study
demonstrates the polyclonal proliferation of microglia after
cerebral ischemia and suggests that clonality contributes to
their functional heterogeneity. Thus, targeting clones with
specific functional phenotypes may have potential for future
therapeutic modulation of microglia after stroke.},
keywords = {Animals / Microglia: pathology / Microglia: physiology /
Microglia: metabolism / Microglia: cytology / Cell
Proliferation / Female / Ischemic Stroke: pathology /
Ischemic Stroke: metabolism / Mice / Cell Communication:
physiology / Mice, Inbred C57BL / Brain Ischemia: pathology
/ Disease Models, Animal / Stroke: pathology / Patch-Clamp
Techniques},
cin = {AG Endres},
ddc = {500},
cid = {I:(DE-2719)1811005},
pnm = {353 - Clinical and Health Care Research (POF4-353)},
pid = {G:(DE-HGF)POF4-353},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:40957877},
pmc = {pmc:PMC12441135},
doi = {10.1038/s41467-025-63949-3},
url = {https://pub.dzne.de/record/281354},
}