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Mechanoinduction of lymph vessel expansion

Planas-Paz, Lara ; Strilić, Boris ; Goedecke, Axel ; Breier, Georg ; Fässler, Reinhard ; Lammert, Eckhard

The EMBO journal, 2012-02, Vol.31 (4), p.788-804 [Periódico revisado por pares]

Chichester, UK: John Wiley & Sons, Ltd

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  • Título:
    Mechanoinduction of lymph vessel expansion
  • Autor: Planas-Paz, Lara ; Strilić, Boris ; Goedecke, Axel ; Breier, Georg ; Fässler, Reinhard ; Lammert, Eckhard
  • Assuntos: Angiogenesis ; Animals ; Biophysics ; Cell growth ; Cell Proliferation ; fluid homeostasis ; Humans ; Integrin beta1 - genetics ; Integrin beta1 - physiology ; Lymphatic system ; lymphatic vessel ; Lymphatic Vessels - cytology ; Mechanotransduction, Cellular ; Mice ; Molecular biology ; mouse embryo ; Phosphorylation ; Signal Transduction ; Vascular Endothelial Growth Factor Receptor-3 - metabolism ; VEGFR3 signalling ; β1 integrin
  • É parte de: The EMBO journal, 2012-02, Vol.31 (4), p.788-804
  • Notas: Supplementary DataSupplementary Movie S1Supplementary Movie S2Review Process File
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    Present address: Department of Pharmacology, Max Planck Institute for Heart and Lung Research, W.G. Kerckhoff-Institute, 61231 Bad Nauheim, Germany
  • Descrição: In the mammalian embryo, few mechanical signals have been identified to influence organ development and function. Here, we report that an increase in the volume of interstitial or extracellular fluid mechanically induces growth of an organ system, that is, the lymphatic vasculature. We first demonstrate that lymph vessel expansion in the developing mouse embryo correlates with a peak in interstitial fluid pressure and lymphatic endothelial cell (LEC) elongation. In ‘loss‐of‐fluid’ experiments, we then show that aspiration of interstitial fluid reduces the length of LECs, decreases tyrosine phosphorylation of vascular endothelial growth factor receptor‐3 (VEGFR3), and inhibits LEC proliferation. Conversely, in ‘gain‐of‐fluid’ experiments, increasing the amount of interstitial fluid elongates the LECs, and increases both VEGFR3 phosphorylation and LEC proliferation. Finally, we provide genetic evidence that β1 integrins are required for the proliferative response of LECs to both fluid accumulation and cell stretching and, therefore, are necessary for lymphatic vessel expansion and fluid drainage. Thus, we propose a new and physiologically relevant mode of VEGFR3 activation, which is based on mechanotransduction and is essential for normal development and fluid homeostasis in a mammalian embryo. Manipulating fluid pressure in the developing lymphatic system demonstrates that lymphatic endothelial cells are responsive to cell stretching, such that increased pressure promotes integrin‐dependent VEGFR3 signalling, cell proliferation, and hence vessel growth.
  • Editor: Chichester, UK: John Wiley & Sons, Ltd
  • Idioma: Inglês
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