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@ARTICLE{Vay:808420,
      author       = {Vay, S. U. and Blaschke, S. and Klein, R. and Fink, Gereon
                      Rudolf and Schroeter, M. and Rueger, M. A.},
      title        = {{M}inocycline mitigates the gliogenic effects of
                      pro-inflammatory cytokines on neural stem cells},
      journal      = {Journal of neuroscience research},
      volume       = {94},
      number       = {2},
      issn         = {0360-4012},
      address      = {New York, NY [u.a.]},
      publisher    = {Wiley-Liss},
      reportid     = {FZJ-2016-02243},
      pages        = {149-160},
      year         = {2016},
      abstract     = {Mobilizing endogenous neural stem cells (NSCs) in the adult
                      brain is designed to enhance the brain's regenerative
                      capacity after cerebral lesions, e.g., as a result of
                      stroke. Cerebral ischemia elicits neuroinflammatory
                      processes affecting NSCs in multiple ways, the precise
                      mechanisms of which currently remain elusive. An inhibitory
                      effect of minocycline on microglia activation, a hallmark of
                      postischemic neuroinflammation, has already been
                      demonstrated in clinical trials, showing minocycline to be
                      safe and potentially effective in ischemic stroke. Here we
                      investigate the direct effects of minocycline and of
                      proinflammatory cytokines on the differentiation potential
                      of NSCs in vitro and in vivo. Primary fetal rat NSCs were
                      treated with minocycline plus a combination of the
                      proinflammatory cytokines tumor necrosis factor-α,
                      interleukin 1β, and interleukin 6. The differentiation fate
                      of NSCs was assessed immunocytochemically. To investigate
                      the effects of minocycline and inflammation in vivo,
                      minocycline or lipopolysaccharides were injected
                      intraperitoneally into adult rats, with subsequent
                      immunohistochemistry. Minocycline alone did not affect the
                      differentiation potential of NSCs in vivo or in vitro. In
                      contrast, proinflammatory cytokines accelerated the
                      differentiation of NSCs, promoting an astrocytic fate while
                      inhibiting neurogenesis in vitro and in vivo. It is
                      interesting to note that minocycline counteracted this
                      cytokine-induced rapid astrocytic differentiation and
                      restored the neurogenic and oligodendrogliogenic potential
                      of NSCs. Data suggest that minocycline antagonizes the rapid
                      glial differentiation induced by proinflammatory cytokines
                      following cerebral ischemia but without having a direct
                      effect on the differentiation potential of NSCs. Thus,
                      minocycline constitutes a promising drug for stroke
                      research, counteracting the detrimental effects of
                      postischemic neuroinflammation in multiple ways.},
      cin          = {INM-3},
      ddc          = {570},
      cid          = {I:(DE-Juel1)INM-3-20090406},
      pnm          = {572 - (Dys-)function and Plasticity (POF3-572)},
      pid          = {G:(DE-HGF)POF3-572},
      typ          = {PUB:(DE-HGF)16},
      UT           = {WOS:000367066600005},
      doi          = {10.1002/jnr.23686},
      url          = {https://juser.fz-juelich.de/record/808420},
}