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10.1038/srep26226

http://scihub22266oqcxt.onion/10.1038/srep26226
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C4872162!4872162 !27194451
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suck abstract from ncbi


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pmid27194451
      Sci+Rep 2016 ; 6 (ä): 26226
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  • Cell-cell contact and matrix adhesion promote ?SMA expression during TGF?1-induced epithelial-myofibroblast transition via Notch and MRTF-A #MMPMID27194451
  • O'Connor JW ; Mistry K ; Detweiler D ; Wang C ; Gomez EW
  • Sci Rep 2016[May]; 6 (ä): 26226 PMID27194451 show ga
  • During epithelial-mesenchymal transition (EMT) epithelial cells lose cell-cell adhesion, exhibit morphological changes, and upregulate the expression of cytoskeletal proteins. Previous studies have demonstrated that complete disruption of cell-cell contact can promote transforming growth factor (TGF)-?1-induced EMT and the expression of the myofibroblast marker alpha smooth muscle actin (?SMA). Furthermore, increased cell spreading mediates TGF?1-induced ?SMA expression during EMT. Here, we sought to examine how the presence of partial cell-cell contacts impacts EMT. A microfabrication approach was employed to decouple the effects of cell-cell contact and cell-matrix adhesion in TGF?1-induced EMT. When cell spreading is controlled, the presence of partial cell-cell contacts enhances expression of ?SMA. Moreover, cell spreading and intercellular contacts together control the subcellular localization of activated Notch1 and myocardin related transcription factor (MRTF)-A. Knockdown of Notch1 or MRTF-A as well as pharmacological inhibition of these pathways abates the cell-cell contact mediated expression of ?SMA. These data suggest that the interplay between cell-matrix adhesion and intercellular adhesion is an important determinant for some aspects of TGF?1-induced EMT.
  • |*Cell Adhesion [MESH]
  • |*Epithelial-Mesenchymal Transition [MESH]
  • |Actins/*metabolism [MESH]
  • |Animals [MESH]
  • |Cells, Cultured [MESH]
  • |Dogs [MESH]
  • |Epithelial Cells/*physiology [MESH]
  • |Extracellular Matrix/*metabolism [MESH]
  • |Gene Knockdown Techniques [MESH]
  • |Mice [MESH]
  • |Myofibroblasts/*physiology [MESH]
  • |Receptor, Notch1/metabolism [MESH]
  • |Trans-Activators/metabolism [MESH]


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