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@ARTICLE{Blaschke:887855,
author = {Blaschke, Stefan J. and Demir, Seda and König, Anna and
Abraham, Jella-Andrea and Vay, Sabine U. and Rabenstein,
Monika and Olschewski, Daniel N. and Hoffmann, Christina and
Hoffmann, Marco and Hersch, Nils and Merkel, Rudolf and
Hoffmann, Bernd and Schroeter, Michael and Fink, Gereon R.
and Rueger, Maria A.},
title = {{S}ubstrate {E}lasticity {E}xerts {F}unctional {E}ffects on
{P}rimary {M}icroglia},
journal = {Frontiers in cellular neuroscience},
volume = {14},
issn = {1662-5102},
address = {Lausanne},
publisher = {Frontiers Research Foundation},
reportid = {FZJ-2020-04481},
pages = {590500},
year = {2020},
abstract = {Microglia—the brain’s primary immune cells—exert a
tightly regulated cascade of pro- and anti-inflammatory
effects upon brain pathology, either promoting regeneration
or neurodegeneration. Therefore, harnessing microglia
emerges as a potential therapeutic concept in neurological
research. Recent studies suggest that—besides being
affected by chemokines and cytokines—various cell entities
in the brain relevantly respond to the mechanical properties
of their microenvironment. For example, we lately reported
considerable effects of elasticity on neural stem cells,
regarding quiescence and differentiation potential. However,
the effects of elasticity on microglia remain to be
explored.Under the hypothesis that the elasticity of the
microenvironment affects key characteristics and functions
of microglia, we established an in vitro model of primary
rat microglia grown in a polydimethylsiloxane (PDMS)
elastomer-based cell culture system. This way, we simulated
the brain’s physiological elasticity range and compared it
to supraphysiological stiffer PDMS controls. We assessed
functional parameters of microglia under “resting”
conditions, as well as when polarized towards a
pro-inflammatory phenotype (M1) by lipopolysaccharide (LPS),
or an anti-inflammatory phenotype (M2) by interleukin-4
(IL-4). Microglia viability was unimpaired on soft
substrates, but we found various significant effects with a
more than two-fold increase in microglia proliferation on
soft substrate elasticities mimicking the brain (relative to
PDMS controls). Furthermore, soft substrates promoted the
expression of the activation marker vimentin in microglia.
Moreover, the M2-marker CD206 was upregulated in parallel to
an increase in the secretion of Insulin-Like Growth Factor-1
(IGF-1). The upregulation of CD206 was abolished by blockage
of stretch-dependent chloride channels. Our data suggest
that the cultivation of microglia on substrates of
brain-like elasticity promotes a basic anti-inflammatory
activation state via stretch-dependent chloride channels.
The results highlight the significance of the omnipresent
but mostly overlooked mechanobiological effects exerted on
microglia and contribute to a better understanding of the
complex spatial and temporal interactions between microglia,
neural stem cells, and glia, in health and disease.},
cin = {INM-3 / IEK-9 / IBI-7 / IBI-2},
ddc = {610},
cid = {I:(DE-Juel1)INM-3-20090406 / I:(DE-Juel1)IEK-9-20110218 /
I:(DE-Juel1)IBI-7-20200312 / I:(DE-Juel1)IBI-2-20200312},
pnm = {572 - (Dys-)function and Plasticity (POF3-572)},
pid = {G:(DE-HGF)POF3-572},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:33250714},
UT = {WOS:000591587300001},
doi = {10.3389/fncel.2020.590500},
url = {https://juser.fz-juelich.de/record/887855},
}