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@ARTICLE{Sridhar:889889,
      author       = {Sridhar, Krishna and Hersch, Nils and Dreissen, Georg and
                      Merkel, Rudolf and Hoffmann, Bernd},
      title        = {{C}alcium mediated functional interplay between myocardial
                      cells upon laser-induced single-cell injury: an in vitro
                      study of cardiac cell death signaling mechanisms},
      journal      = {Cell communication and signaling},
      volume       = {18},
      number       = {1},
      issn         = {1478-811X},
      address      = {London},
      publisher    = {Biomed Central},
      reportid     = {FZJ-2021-00497},
      pages        = {191},
      year         = {2020},
      abstract     = {BackgroundThe electromechanical function of myocardial
                      tissue depends on the intercellular communication between
                      cardiomyocytes (CMs) as well as their crosstalk with other
                      cell types. Cell injury, and subsequent death trigger
                      inflammation as in myocardial infarction (MI) resulting in
                      myocardial remodeling. Although mechanisms underlying
                      myocardial cell death have been studied so far, the
                      signaling events following single cell death and spontaneous
                      response of connected cells in the myocardial tissue is
                      still barely understood.MethodsHere, we investigated the
                      effect of laser-induced single cell death on Calcium (Ca2+)
                      concentrations and transport in myocardial cell clusters in
                      vitro. Spatial and temporal changes in intracellular Ca2+
                      concentrations [Ca2+]i were studied using a fluorescent
                      calcium indicator, Fluo-4AM. Spontaneous signaling events
                      following cell death were studied in rat embryonic
                      cardiomyocytes and non-myocytes using separate cell culture
                      systems.ResultsCell death triggered spontaneous increase in
                      intracellular Ca2+ levels ([Ca2+]i) of surrounding cells.
                      The spread of the observed propagating Ca2+ signal was slow
                      and sustained in myocytes while it was rapid and transient
                      in fibroblasts (Fbs). Further, sustained high Ca2+ levels
                      temporarily impaired the contractility in CMs. The cell-type
                      specific effect of ablation was confirmed using separate
                      cultures of CMs and Fbs. Comparing Ca2+ propagation speed in
                      myocytes and fibroblasts, we argue for a diffusion-driven
                      Ca2+ propagation in myocytes, but not in fibroblasts. Radial
                      and sequential Ca2+ diffusion across the CMs through
                      cell–cell contacts and presence of Cx43-based
                      intercellular junctions indicated a gap junction flow of
                      Ca2+.ConclusionsThese findings illustrate the spontaneous
                      Ca2+-mediated functional interplay in myocardial cell
                      clusters upon mechanical injury and, further, the difference
                      in Ca2+ signaling in cardiomyocytes and fibroblasts.},
      cin          = {IBI-2},
      ddc          = {570},
      cid          = {I:(DE-Juel1)IBI-2-20200312},
      pnm          = {552 - Engineering Cell Function (POF3-552)},
      pid          = {G:(DE-HGF)POF3-552},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {33371897},
      UT           = {WOS:000603349100001},
      doi          = {10.1186/s12964-020-00689-5},
      url          = {https://juser.fz-juelich.de/record/889889},
}