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10.1038/srep23770

http://scihub22266oqcxt.onion/10.1038/srep23770
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C4820704!4820704 !27044328
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suck abstract from ncbi


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pmid27044328
      Sci+Rep 2016 ; 6 (ä): 23770
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  • BET Bromodomain Suppression Inhibits VEGF-induced Angiogenesis and Vascular Permeability by Blocking VEGFR2-mediated Activation of PAK1 and eNOS #MMPMID27044328
  • Huang M ; Qiu Q ; Xiao Y ; Zeng S ; Zhan M ; Shi M ; Zou Y ; Ye Y ; Liang L ; Yang X ; Xu H
  • Sci Rep 2016[Apr]; 6 (ä): 23770 PMID27044328 show ga
  • The tyrosine kinase receptor vascular endothelial growth factor receptor 2 (VEGFR2) is a critical modulator of angiogenesis. Increasing evidence indicate the important role of bromodomain and extra-terminal domain (BET) of chromatin adaptors in regulating tumor growth and inflammatory response. However, whether BET proteins have a role in angiogenesis and endothelial permeability is unclear. In this study, we observed that treatment with JQ1, a specific BET inhibitor, suppressed in vitro tube formation of human umbilical vein endothelial cells (HUVECs) and in vivo angiogenesis in a Matrigel plug and oxygen-induced retinopathy neovascularization. JQ1 attenuated the VEGF-induced decrease in TEER in HUVECs and prevented Evans blue dye leakage in the VEGF-induced Miles assay in athymic Balb/c nude mice. BET inhibition with JQ1 or shRNA for Brd2 or Brd4 suppressed VEGF-induced migration, proliferation, and stress fiber formation of HUVECs. Furthermore, BET inhibition suppressed phosphorylation of VEGFR2 and PAK1, as well as eNOS activation in VEGF-stimulated HUVECs. Inhibition with VEGFR2 and PAK1 also reduced migration and proliferation, and attenuated the VEGF-induced decrease in TEER. Thus, our observations suggest the important role of BET bromodomain in regulating VEGF-induced angiogenesis. Strategies that target the BET bromodomain may provide a new therapeutic approach for angiogenesis-related diseases.
  • |Angiogenesis Inducing Agents/pharmacology [MESH]
  • |Animals [MESH]
  • |Cell Movement [MESH]
  • |Cell Proliferation [MESH]
  • |Chemotaxis [MESH]
  • |Human Umbilical Vein Endothelial Cells [MESH]
  • |Humans [MESH]
  • |Hyperoxia/metabolism [MESH]
  • |Inflammation [MESH]
  • |Male [MESH]
  • |Mice [MESH]
  • |Mice, Inbred C57BL [MESH]
  • |Mice, Nude [MESH]
  • |Neovascularization, Pathologic/*physiopathology [MESH]
  • |Nitric Oxide Synthase Type III/*metabolism [MESH]
  • |Oxygen/chemistry [MESH]
  • |Permeability [MESH]
  • |Phosphorylation [MESH]
  • |Protein Domains [MESH]
  • |RNA, Small Interfering/metabolism [MESH]
  • |Retroviridae/genetics [MESH]
  • |Vascular Endothelial Growth Factor A/*pharmacology [MESH]
  • |Vascular Endothelial Growth Factor Receptor-2/*metabolism [MESH]


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