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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},
}