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@ARTICLE{Will:284769,
      author       = {P. A. Will and K. Kilian and K. Bieback and F. Fricke$^*$
                      and J. E. Berner and U. Kneser and C. Hirche},
      title        = {{L}ymphedema-{A}ssociated {F}ibroblasts {A}re {R}elated to
                      {F}ibrosis and {S}tage {P}rogression in {P}atients and a
                      {M}urine {M}icrosurgical {M}odel},
      journal      = {Plastic and reconstructive surgery},
      volume       = {154},
      number       = {4},
      issn         = {0032-1052},
      address      = {[Erscheinungsort nicht ermittelbar]},
      publisher    = {Ovid},
      reportid     = {DKFZ-2023-02080},
      pages        = {688e-700e},
      year         = {2024},
      note         = {2024 Oct 1;154(4):688e-700e},
      abstract     = {The driver of secondary lymphedema (SL) progression is
                      chronic inflammation, which promotes fibrosis. Despite
                      advances in preclinical research, a specific effector cell
                      subpopulation as a biomarker for therapy response or stage
                      progression is still missing for SL.Whole skin samples of 35
                      murine subjects of a microsurgical-induced SL model and 12
                      patients with SL were collected and their fibroblasts were
                      isolated. These lymphedema-derived fibroblasts (LAF) were
                      cultured in a collagen I-poly-D-Lysine 3D hydrogel to mimic
                      skin conditions. Fibroblasts from non-lymphedema skin were
                      used as negative control and TGF-β-stimulated fibroblasts
                      were used to recreate profibrotic myofibroblasts.
                      Quantitative immunocytofluorescence confocal microscopy
                      analysis and invasion functional assays were performed in
                      all subpopulations and statistically compared.In contrast to
                      normal skin fibroblasts, LAF exhibit α-SMA-positive stress
                      fibers and a reduced number of tight junctions in 3D
                      hydrogel conditions. The switch from normal E-cadherin high
                      phenotype to an N-cadherin high-E-cadherin low morphology
                      suggests epithelial to mesenchymal transition for expansion
                      and proliferation. This pathological behavior of LAF was
                      confirmed by live cell imaging analysis of invasion assays.
                      The significant activation of markers of the TGFBR2-Smad
                      pathway and collagen synthesis (HSP-47) in LAF supports EMT
                      phenotypic changes and previous findings relating to TGF-β1
                      and fibrosis with lymphedema.A characteristic SL
                      myofibroblast subpopulation was identified and
                      translationally related to fibrosis and TGF-β1-associated
                      stage progression. This SL-related subpopulation was termed
                      lymphedema-associated fibroblasts. A comprehensive
                      stage-related characterization is required to validate LAF
                      as a reliable biomarker for SL disease progression.},
      cin          = {F210},
      ddc          = {610},
      cid          = {I:(DE-He78)F210-20160331},
      pnm          = {316 - Infektionen, Entzündung und Krebs (POF4-316)},
      pid          = {G:(DE-HGF)POF4-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37832143},
      doi          = {10.1097/PRS.0000000000011141},
      url          = {https://inrepo02.dkfz.de/record/284769},
}