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@ARTICLE{Rakers:140510,
      author       = {Rakers, Cordula and Schleif, Melvin and Blank, Nelli and
                      Matušková, Hana and Ulas, Thomas and Händler, Kristian
                      and Torres, Santiago Valle and Schumacher, Toni and Tai,
                      Khalid and Schultze, Joachim L and Jackson, Walker S and
                      Petzold, Gabor Claus Julius Peter},
      title        = {{S}troke target identification guided by astrocyte
                      transcriptome analysis.},
      journal      = {Glia},
      volume       = {67},
      number       = {4},
      issn         = {0894-1491},
      address      = {Bognor Regis [u.a.]},
      publisher    = {Wiley-Liss},
      reportid     = {DZNE-2020-06832},
      pages        = {619-633},
      year         = {2019},
      abstract     = {Astrocytes support normal brain function, but may also
                      contribute to neurodegeneration when they become reactive
                      under pathological conditions such as stroke. However, the
                      molecular underpinnings of this context-dependent interplay
                      between beneficial and detrimental properties in reactive
                      astrogliosis have remained incompletely understood.
                      Therefore, using the RiboTag technique, we immunopurified
                      translating mRNAs specifically from astrocytes 72 hr after
                      transient middle cerebral artery occlusion in mice (tMCAO),
                      thereby generating a stroke-specific astroglial translatome
                      database. We found that compared to control brains, reactive
                      astrocytes after tMCAO show an enrichment of transcripts
                      linked to the A2 phenotype, which has been associated with
                      neuroprotection. However, we found that astrocytes also
                      upregulate a large number of potentially neurotoxic genes.
                      In total, we identified the differential expression of 1,003
                      genes and 38 transcription factors, of which Stat3, Sp1, and
                      Spi1 were the most prominent. To further explore the effects
                      of Stat3-mediated pathways on stroke pathogenesis, we
                      subjected mice with an astrocyte-specific conditional
                      deletion of Stat3 to tMCAO, and found that these mice have
                      reduced stroke volume and improved motor outcome 72 hr
                      after focal ischemia. Taken together, our study extends the
                      emerging database of novel astrocyte-specific targets for
                      stroke therapy, and supports the role of astrocytes as
                      critical safeguards of brain function in health and
                      disease.},
      keywords     = {Animals / Astrocytes: metabolism / Computational Biology /
                      Connexin 43: genetics / Connexin 43: metabolism / Disease
                      Models, Animal / Female / Galectin 3: genetics / Galectin 3:
                      metabolism / Gene Expression Profiling: methods / Gene
                      Expression Regulation: genetics / Immunoprecipitation /
                      Infarction, Middle Cerebral Artery: pathology / Infarction,
                      Middle Cerebral Artery: physiopathology / Lipocalin-2:
                      genetics / Lipocalin-2: metabolism / Luminescent Proteins:
                      genetics / Luminescent Proteins: metabolism / Male / Mice /
                      Mice, Inbred C57BL / Mice, Transgenic / Nerve Tissue
                      Proteins: metabolism / Rhombencephalon: pathology / Rotarod
                      Performance Test / STAT3 Transcription Factor: genetics /
                      STAT3 Transcription Factor: metabolism / Connexin 43 (NLM
                      Chemicals) / Galectin 3 (NLM Chemicals) / Lipocalin-2 (NLM
                      Chemicals) / Luminescent Proteins (NLM Chemicals) / Nerve
                      Tissue Proteins (NLM Chemicals) / STAT3 Transcription Factor
                      (NLM Chemicals) / Stat3 protein, mouse (NLM Chemicals)},
      cin          = {AG Petzold / AG Jackson / AG Krauß / AG Schultze},
      ddc          = {610},
      cid          = {I:(DE-2719)1013020 / I:(DE-2719)1013019 /
                      I:(DE-2719)1011006 / I:(DE-2719)1013038},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342) / 344
                      - Clinical and Health Care Research (POF3-344)},
      pid          = {G:(DE-HGF)POF3-342 / G:(DE-HGF)POF3-344},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30585358},
      doi          = {10.1002/glia.23544},
      url          = {https://pub.dzne.de/record/140510},
}