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@ARTICLE{Pekna:181679,
author = {M. Pekna and S. Siqin$^*$ and Y. de Pablo and A. Stokowska
and Å. Torinsson Naluai and M. Pekny},
title = {{A}strocyte {R}esponses to {C}omplement {P}eptide {C}3a are
{H}ighly {C}ontext-{D}ependent.},
journal = {Neurochemical research},
volume = {48},
number = {4},
issn = {0364-3190},
address = {Dordrecht [u.a.]},
publisher = {Springer Science + Business Media B.V},
reportid = {DKFZ-2022-02159},
pages = {1233-1241},
year = {2023},
note = {2023 Apr;48(4):1233-1241},
abstract = {Astrocytes perform a range of homeostatic and regulatory
tasks that are critical for normal functioning of the
central nervous system. In response to an injury or disease,
astrocytes undergo a pronounced transformation into a
reactive state that involves changes in the expression of
many genes and dramatically changes astrocyte morphology and
functions. This astrocyte reactivity is highly dependent on
the initiating insult and pathological context. C3a is a
peptide generated by the proteolytic cleavage of the third
complement component. C3a has been shown to exert
neuroprotective effects, stimulate neural plasticity and
promote astrocyte survival but can also contribute to
synapse loss, Alzheimer's disease type neurodegeneration and
blood-brain barrier dysfunction. To test the hypothesis that
C3a elicits differential effects on astrocytes depending on
their reactivity state, we measured the expression of Gfap,
Nes, C3ar1, C3, Ngf, Tnf and Il1b in primary mouse cortical
astrocytes after chemical ischemia, after exposure to
lipopolysaccharide (LPS) as well as in control naïve
astrocytes. We found that C3a down-regulated the expression
of Gfap, C3 and Nes in astrocytes after ischemia. Further,
C3a increased the expression of Tnf and Il1b in naive
astrocytes and the expression of Nes in astrocytes exposed
to LPS but did not affect the expression of C3ar1 or Ngf.
Jointly, these results provide the first evidence that the
complement peptide C3a modulates the responses of astrocytes
in a highly context-dependent manner.},
keywords = {Gene expression (Other) / Glia (Other) / Ischemia (Other) /
Lipopolysaccharide (Other) / Neurodegeneration (Other)},
cin = {F200},
ddc = {610},
cid = {I:(DE-He78)F200-20160331},
pnm = {316 - Infektionen, Entzündung und Krebs (POF4-316)},
pid = {G:(DE-HGF)POF4-316},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:36097103},
doi = {10.1007/s11064-022-03743-5},
url = {https://inrepo02.dkfz.de/record/181679},
}