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@ARTICLE{Esser:1007122,
      author       = {Esser, Lisann and Springer, Ronald and Dreissen, Georg and
                      Lövenich, Lukas and Konrad, Jens and Hampe, Nico and
                      Merkel, Rudolf and Hoffmann, Bernd and Noetzel, Erik},
      title        = {{E}lastomeric {P}illar {C}ages {M}odulate {A}ctomyosin
                      {C}ontractility of {E}pithelial {M}icrotissues by
                      {S}ubstrate {S}tiffness and {T}opography},
      journal      = {Cells},
      volume       = {12},
      number       = {9},
      issn         = {2073-4409},
      address      = {Basel},
      publisher    = {MDPI},
      reportid     = {FZJ-2023-01956},
      pages        = {1256 -},
      year         = {2023},
      abstract     = {Cell contractility regulates epithelial tissue geometry
                      development and homeostasis. The underlying
                      mechanobiological regulation circuits are poorly understood
                      and experimentally challenging. We developed an elastomeric
                      pillar cage (EPC) array to quantify cell contractility as a
                      mechanoresponse of epithelial microtissues to substrate
                      stiffness and topography. The spatially confined EPC
                      geometry consisted of 24 circularly arranged slender pillars
                      (1.2 MPa, height: 50 µm; diameter: 10 µm, distance: 5
                      µm). These high-aspect-ratio pillars were confined at both
                      ends by planar substrates with different stiffness
                      (0.15–1.2 MPa). Analytical modeling and finite elements
                      simulation retrieved cell forces from pillar displacements.
                      For evaluation, highly contractile myofibroblasts and
                      cardiomyocytes were assessed to demonstrate that the EPC
                      device can resolve static and dynamic cellular force modes.
                      Human breast (MCF10A) and skin (HaCaT) cells grew as
                      adherence junction-stabilized 3D microtissues within the EPC
                      geometry. Planar substrate areas triggered the spread of
                      monolayered clusters with substrate stiffness-dependent
                      actin stress fiber (SF)-formation and substantial
                      single-cell actomyosin contractility (150–200 nN). Within
                      the same continuous microtissues, the pillar-ring topography
                      induced the growth of bilayered cell tubes. The low
                      effective pillar stiffness overwrote cellular sensing of the
                      high substrate stiffness and induced SF-lacking roundish
                      cell shapes with extremely low cortical actin tension
                      (11–15 nN). This work introduced a versatile biophysical
                      tool to explore mechanobiological regulation circuits
                      driving low- and high-tensional states during microtissue
                      development and homeostasis. EPC arrays facilitate
                      simultaneously analyzing the impact of planar substrate
                      stiffness and topography on microtissue contractility, hence
                      microtissue geometry and function.},
      cin          = {IBI-2},
      ddc          = {570},
      cid          = {I:(DE-Juel1)IBI-2-20200312},
      pnm          = {5243 - Information Processing in Distributed Systems
                      (POF4-524) / DFG project 273723265 - Mechanosensation und
                      Mechanoreaktion in epidermalen Systemen},
      pid          = {G:(DE-HGF)POF4-5243 / G:(GEPRIS)273723265},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {37174659},
      UT           = {WOS:000987253300001},
      doi          = {10.3390/cells12091256},
      url          = {https://juser.fz-juelich.de/record/1007122},
}