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@ARTICLE{Celikkaya:140480,
      author       = {Celikkaya, Hilal and Cosacak, Mehmet Ilyas and
                      Papadimitriou, Christos and Popova, Stanislava and
                      Bhattarai, Prabesh and Biswas, Srijeeta Nag and Siddiqui,
                      Tohid and Wistorf, Sabrina and Nevado-Alcalde, Isabel and
                      Naumann, Lisa and Mashkaryan, Violeta and Brandt, Kerstin
                      and Freudenberg, Uwe and Werner, Carsten and Kizil, Caghan},
      title        = {{GATA}3 {P}romotes the {N}eural {P}rogenitor {S}tate but
                      {N}ot {N}eurogenesis in 3{D} {T}raumatic {I}njury {M}odel of
                      {P}rimary {H}uman {C}ortical {A}strocytes.},
      journal      = {Frontiers in cellular neuroscience},
      volume       = {13},
      issn         = {1662-5102},
      address      = {Lausanne},
      publisher    = {Frontiers Research Foundation},
      reportid     = {DZNE-2020-06802},
      pages        = {23},
      year         = {2019},
      abstract     = {Astrocytes are abundant cell types in the vertebrate
                      central nervous system and can act as neural stem cells in
                      specialized niches where they constitutively generate new
                      neurons. Outside the stem cell niches, however, these glial
                      cells are not neurogenic. Although injuries in the mammalian
                      central nervous system lead to profound proliferation of
                      astrocytes, which cluster at the lesion site to form a
                      gliotic scar, neurogenesis does not take place. Therefore, a
                      plausible regenerative therapeutic option is to coax the
                      endogenous reactive astrocytes to a pre-neurogenic
                      progenitor state and use them as an endogenous reservoir for
                      repair. However, little is known on the mechanisms that
                      promote the neural progenitor state after injuries in
                      humans. Gata3 was previously found to be a mechanism that
                      zebrafish brain uses to injury-dependent induction of neural
                      progenitors. However, the effects of GATA3 in human
                      astrocytes after injury are not known. Therefore, in this
                      report, we investigated how overexpression of GATA3 in
                      primary human astrocytes would affect the neurogenic
                      potential before and after injury in 2D and 3D cultures. We
                      found that primary human astrocytes are unable to induce
                      GATA3 after injury. Lentivirus-mediated overexpression of
                      GATA3 significantly increased the number of GFAP/SOX2 double
                      positive astrocytes and expression of pro-neural factor
                      ASCL1, but failed to induce neurogenesis, suggesting that
                      GATA3 is required for enhancing the neurogenic potential of
                      primary human astrocytes and is not sufficient to induce
                      neurogenesis alone.},
      cin          = {AG Kizil / Dresden Pre 2020 / AG Kempermann 1},
      ddc          = {610},
      cid          = {I:(DE-2719)1710007 / I:(DE-2719)6000013 /
                      I:(DE-2719)1710001},
      pnm          = {341 - Molecular Signaling (POF3-341) / 342 - Disease
                      Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-341 / G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30809125},
      pmc          = {pmc:PMC6380212},
      doi          = {10.3389/fncel.2019.00023},
      url          = {https://pub.dzne.de/record/140480},
}