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@ARTICLE{Vay:874938,
      author       = {Vay, Sabine Ulrike and Flitsch, Lea Jessica and Rabenstein,
                      Monika and Monière, Helena and Jakovcevski, Igor and
                      Andjus, Pavle and Bijelic, Dunja and Blaschke, Stefan and
                      Walter, Helene Luise and Fink, Gereon Rudolf and Schroeter,
                      Michael and Rueger, Maria Adele},
      title        = {{T}he impact of hyperpolarization-activated cyclic
                      nucleotide-gated ({HCN}) and voltage-gated potassium
                      {KCNQ}/{K}v7 channels on primary microglia function},
      journal      = {Journal of neuroinflammation},
      volume       = {17},
      number       = {1},
      issn         = {1742-2094},
      address      = {London},
      publisher    = {BioMed Central},
      reportid     = {FZJ-2020-01710},
      pages        = {100},
      year         = {2020},
      abstract     = {BackgroundMicroglia are essential to maintain cell
                      homeostasis in the healthy brain and are activated after
                      brain injury. Upon activation, microglia polarize towards
                      different phenotypes. The course of microglia activation is
                      complex and depends on signals in the surrounding milieu.
                      Recently, it has been suggested that microglia respond to
                      ion currents, as a way of regulating their activity and
                      function.Methods and resultsUnder the hypothesis that HCN
                      and KCNQ/Kv7 channels impact on microglia, we studied
                      primary rat microglia in the presence or absence of specific
                      pharmacological blockade or RNA silencing. Primary microglia
                      expressed the subunits HCN1-4, Kv7.2, Kv7.3, and Kv7.5. The
                      expression of HCN2, as well as Kv7.2 and Kv7.3, varied among
                      different microglia phenotypes. The pharmacological blockade
                      of HCN channels by ZD7288 resulted in cell depolarization
                      with slowly rising intracellular calcium levels, leading to
                      enhanced survival and reduced proliferation rates of resting
                      microglia. Furthermore, ZD7288 treatment, as well as
                      knockdown of HCN2 RNA by small interfering RNA, resulted in
                      an attenuation of later microglia activation—both towards
                      the anti- and pro-inflammatory phenotype. However, HCN
                      channel inhibition enhanced the phagocytic capacity of
                      IL4-stimulated microglia. Blockade of Kv7/KCNQ channel by
                      XE-991 exclusively inhibited the migratory capacity of
                      resting microglia.ConclusionThese observations suggest that
                      the HCN current contributes to various microglia functions
                      and impacts on the course of microglia activation, while the
                      Kv7/KCNQ channels affect microglia migration. Characterizing
                      the role of HCN channels in microglial functioning may offer
                      new therapeutic approaches for targeted modulation of
                      neuroinflammation as a hallmark of various neurological
                      disorders.},
      cin          = {INM-3},
      ddc          = {610},
      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},
      pubmed       = {pmid:32248813},
      UT           = {WOS:000525175500001},
      doi          = {10.1186/s12974-020-01779-4},
      url          = {https://juser.fz-juelich.de/record/874938},
}