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Sökning: WFRF:(Scallan Joshua)

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1.
  • Sabine, Amelie, et al. (författare)
  • FOXC2 and fluid shear stress stabilize postnatal lymphatic vasculature
  • 2015
  • Ingår i: Journal of Clinical Investigation. - 0021-9738 .- 1558-8238. ; 125:10, s. 3861-3877
  • Tidskriftsartikel (refereegranskat)abstract
    • Biomechanical forces, such as fluid shear stress, govern multiple aspects of endothelial cell biology. In blood vessels, disturbed flow is associated with vascular diseases, such as atherosclerosis, and promotes endothelial cell proliferation and apoptosis. Here, we identified an important role for disturbed flow in lymphatic vessels, in which it cooperates with the transcription factor FOXC2 to ensure lifelong stability of the lymphatic vasculature. In cultured lymphatic endothelial cells, FOXC2 inactivation conferred abnormal shear stress sensing, promoting junction disassembly and entry into the cell cycle. Loss of FOXC2-dependent quiescence was mediated by the Hippo pathway transcriptional coactivator TAZ and, ultimately, led to cell death. In murine models, inducible deletion of Foxc2 within the lymphatic vasculature led to cell-cell junction defects, regression of valves, and focal vascular lumen collapse, which triggered generalized lymphatic vascular dysfunction and lethality. Together, our work describes a fundamental mechanism by which FOXC2 and oscillatory shear stress maintain lymphatic endothelial cell quiescence through intercellular junction and cytoskeleton stabilization and provides an essential link between biomechanical forces and endothelial cell identity that is necessary for postnatal vessel homeostasis. As FOXC2 is mutated in lymphedema-distichiasis syndrome, our data also underscore the role of impaired mechanotransduction in the pathology of this hereditary human disease.
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2.
  • Vestweber, Dietmar, et al. (författare)
  • Report from the 2023 workshop on endothelial permeability, edema and inflammation
  • 2023
  • Ingår i: Nature Cardiovascular Research. - : Springer Nature. - 2731-0590. ; 2:12, s. 1120-1124
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
    • A key consequence of increased and sustained vascular permeability in several inflammatory and cardiovascular disorders is the development of interstitial protein-rich proinflammatory edema. This response remains poorly understood mechanistically and its potential adverse effect on local and systemic diseases is often underestimated. To discuss current findings and identify crucial unresolved questions, a workshop was held in Berlin from 12-15 April 2023. Key topics that were discussed included regulation of endothelial cell junctions, neutrophil-dependent vascular leakage, resolution of edema, exemplar diseases, and anti-edema therapies. This report is a summary of the meeting.
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