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@ARTICLE{HerasBautista:861506,
      author       = {Heras-Bautista, Carlos O. and Mikhael, Nelly and Lam,
                      Jennifer and Shinde, Vaibhav and Katsen-Globa, Alisa and
                      Dieluweit, Sabine and Molcanyi, Marek and Uvarov, Vladimir
                      and Jütten, Peter and Sahito, Raja G. A. and Mederos-Henry,
                      Francisco and Piechot, Alexander and Brockmeier, Konrad and
                      Hescheler, Jürgen and Sachinidis, Agapios and Pfannkuche,
                      Kurt},
      title        = {{C}ardiomyocytes facing fibrotic conditions re-express
                      extracellular matrix transcripts7},
      journal      = {Acta biomaterialia},
      volume       = {89},
      issn         = {1742-7061},
      address      = {[Amsterdam]},
      publisher    = {Elsevier},
      reportid     = {FZJ-2019-01964},
      pages        = {180-192},
      year         = {2019},
      abstract     = {Pathophysiological conditions, such as myocardial
                      infarction and mechanical overload affect the mammalian
                      heart integrity, leading to a stiffened fibrotic tissue.
                      With respect to the pathophysiology of cardiac fibrosis but
                      also in the limelight of upcoming approaches of cardiac cell
                      therapy it is of interest to decipher the interaction of
                      cardiomyocytes with fibrotic matrix. Therefore, we designed
                      a hydrogel-based model to engineer fibrotic tissue in vitro
                      as an approach to predict the behavior of cardiomyocytes
                      facing increased matrix rigidity. Here, we generated pure
                      induced pluripotent stem cell-derived cardiomyocytes and
                      cultured them on engineered polyacrylamide hydrogels
                      matching the elasticities of healthy as well as fibrotic
                      cardiac tissue. Only in cardiomyocytes cultured on matrices
                      with fibrotic-like elasticity, transcriptional profiling
                      revealed a substantial up-regulation of a whole panel of
                      cardiac fibrosis-associated transcripts, including collagen
                      I and III, decorin, lumican, and periostin. In addition,
                      matrix metalloproteinases and their inhibitors, known to be
                      essential in cardiac remodeling, were found to be elevated
                      as well as insulin-like growth factor 2. Control experiments
                      with primary cardiac fibroblasts were analyzed and did not
                      show comparable behavior. In conclusion, we do not only
                      present a snapshot on the transcriptomic fingerprint
                      alterations in cardiomyocytes under pathological conditions
                      but also provide a new reproducible approach to study the
                      effects of fibrotic environments to various cell types.},
      cin          = {ICS-7},
      ddc          = {530},
      cid          = {I:(DE-Juel1)ICS-7-20110106},
      pnm          = {552 - Engineering Cell Function (POF3-552)},
      pid          = {G:(DE-HGF)POF3-552},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30862552},
      UT           = {WOS:000466258600015},
      doi          = {10.1016/j.actbio.2019.03.017},
      url          = {https://juser.fz-juelich.de/record/861506},
}