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@ARTICLE{Sattler:169897,
      author       = {K. Sattler and I. El-Battrawy and L. Cyganek and S. Lang
                      and H. Lan and X. Li and Z. Zhao and J. Utikal$^*$ and T.
                      Wieland and M. Borggrefe and X. Zhou and I. Akin},
      title        = {{TRPV}1 activation and internalization is part of the
                      {LPS}-induced inflammation in human i{PSC}-derived
                      cardiomyocytes.},
      journal      = {Scientific reports},
      volume       = {11},
      number       = {1},
      issn         = {2045-2322},
      address      = {[London]},
      publisher    = {Macmillan Publishers Limited, part of Springer Nature},
      reportid     = {DKFZ-2021-01631},
      pages        = {14689},
      year         = {2021},
      abstract     = {The non-selective cation channel transient receptor
                      potential vanilloid 1 (TRPV1) is expressed throughout the
                      cardiovascular system. Recent evidence shows a role for
                      TRPV1 in inflammatory processes. The role of TRPV1 for
                      myocardial inflammation has not been established yet. Human
                      induced pluripotent stem cell (iPSC)-derived cardiomyocytes
                      (hiPSC-CM) from 4 healthy donors were incubated with
                      lipopolysaccharides (LPS, 6 h), TRPV1 agonist capsaicin
                      (CAP, 20 min) or the antagonist capsazepine (CPZ, 20 min).
                      TRPV1 expression was studied by PCR and western blotting.
                      TRPV1 internalization was analyzed by immunofluorescence.
                      Interleukin-6 (IL-6) secretion and phosphorylation of JNK,
                      p38 and ERK were determined by ELISA. TRPV1-associated ion
                      channel current was measured by patch clamp. TRPV1-mRNA and
                      -protein were expressed in hiPSC-CM. TRPV1 was localized in
                      the plasma membrane. LPS significantly increased secretion
                      of IL-6 by 2.3-fold, which was prevented by pre-incubation
                      with CPZ. LPS induced TRPV1 internalization. Phosphorylation
                      levels of ERK, p38 or JNK were not altered by TRPV1
                      stimulation or inhibition. LPS and IL-6 significantly
                      lowered TRPV1-mediated ion channel current. TRPV1 mediates
                      the LPS-induced inflammation in cardiomyocytes, associated
                      with changes of cellular electrophysiology. LPS-induced
                      inflammation results in TRPV1 internalization. Further
                      studies have to examine the underlying pathways and the
                      clinical relevance of these findings.},
      cin          = {A370},
      ddc          = {600},
      cid          = {I:(DE-He78)A370-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34282193},
      doi          = {10.1038/s41598-021-93958-3},
      url          = {https://inrepo02.dkfz.de/record/169897},
}